Clinical characteristics and outcome of malaria-associated acute kidney injury in adult patients: a systematic review and meta analysis

Abstract

Background

Malaria-associated acute kidney injury (MAKI) represents a severe complication of malaria, increasingly documented in both Plasmodium falciparum and Plasmodium vivax infections across endemic regions.

Methods

A systematic review and metaanalysis using PubMed, EMBASE, and Cochrane CENTRAL was conducted to identify studies published between 2000 and 2024. This review evaluates the existing literature on MAKI in adult population, aiming to synthesize data on demographics, Plasmodium species, kidney involvement, dialysis need, mortality, kidney histopathology, and long-term kidney outcomes.

Results

The review included 25 studies with 2,094 MAKI patients predominantly from South Asia, especially India followed by Pakistan and Thailand. Plasmodium falciparum was the most common species implicated, though severe AKI due to P. vivax was increasingly reported. AKI definitions varied, using serum creatinine thresholds or classifications like KDIGO, RIFLE, and WHO. The incidence of MAKI ranged from 2.4 to 45.5%, rising to as high as 77% among patients with severe malaria. The pooled incidence of AKI among adults patients with malaria was 26.5% (95% CI 19.8–34.4; I² = 97%). Dialysis was required in 20–90% of cases. The mean creatinine ranged from 1.5 to over 10 mg/dL. The pooled mortality among adults MAKI patients was 19.2% (95% CI 12.9–27.7%). Mortality varied from 5 to 52%, higher in cases with delayed presentation, cerebral malaria, sepsis, need for mechanical ventilation, metabolic acidosis, and multiorgan failure. Among 95 biopsied cases, acute tubular necrosis was most common but vascular injuries like thrombotic microangiopathy and acute cortical necrosis were strongly associated with P. vivax. Long-term data were limited, but 5–20% of patients developed chronic kidney disease or kidney failure. Sub-Saharan Africa remained underrepresented despite its high malaria burden.

Conclusion

MAKI is a severe complication of malaria with regional variation in species, outcomes, and care access. Improved diagnostics, timely dialysis, and long-term nephrology follow-up are essential in endemic regions.

Supplementary Information

The online version contains supplementary material available at 10.1186/s12936-025-05777-w.

Background

Acute kidney injury (AKI) is a critical global health concern with disproportionately high morbidity and mortality, particularly in low- and middle-income countries, where infectious diseases dominate its aetiology. In these regions, community-acquired AKI often arises from preventable or treatable infections, such as leptospirosis, dengue, scrub typhus, and importantly, malaria [1]. Among these, malaria has emerged as a significant and increasingly recognized cause of AKI [2], especially in endemic settings, yet its kidney manifestations and long term outcomes remain inadequately understood and inconsistently reported. According to the WHO’s World Malaria Report 2024, an estimated 263 million malaria infections and 597,000 deaths occurred globally in 2023 [3], with the vast majority reported from sub-Saharan Africa, Central and South America and Southeast Asia [3]. Among the five Plasmodium species known to infect humans Plasmodium falciparum is most strongly associated with severe complications [4], including cerebral malaria, severe anaemia, pulmonary oedema, haemoglobinuria, and AKI. Plasmodium vivax, long considered less virulent, has also been increasingly implicated in severe complications, including kidney involvement, challenging traditional species-based risk paradigms [5].

Kidney manifestations in malaria range from mild urinary abnormalities to severe AKI requiring kidney replacement therapy (KRT). AKI occurs in up to 40–45% of adults with severe malaria and is associated with high mortality rates [6]. In non-immune populations, such as travellers returning from endemic areas, AKI has been reported in 34–52% of P. falciparum infections further emphasizing the global relevance of this complication [7]. Epidemiological data are hindered by wide heterogeneity in study designs, diagnostic criteria and definitions of AKI. Thresholds used to identify AKI whether based on serum creatinine, urine output, or standardized classifications, such as World Health Organization (WHO), RIFLE (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease) classification, Acute Kidney Injury Network (AKIN), Kidney Disease: Improving Global Outcomes (KDIGO) vary considerably across studies, complicating efforts to ascertain true incidence rates.

The International Society of Nephrology’s 0by25 initiative emphasizes the urgency of addressing preventable AKI deaths worldwide [8]. A nuanced understanding of the clinical course, kidney involvement, risk factors, and outcomes of Malaria-associated acute kidney injury (MAKI) is essential to inform context-specific prevention and treatment strategies.

A systematic review and meta-analysis was conducted to evaluate to synthesize data on demographics, kidney involvement, dialysis need, mortality, kidney histopathology, and long-term kidney outcomes in adult malaria patients.

Methods

Study design and registration

A systematic review in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA) guidelines was conducted [9]. The review protocol was prospectively registered in the International Prospective Register of Systematic Reviews (PROSPERO; registration number: CRD42024585274).

Eligibility criteria

Peer-reviewed studies were included if they, specifically reported on clinical characteristics and outcomes of AKI associated with malaria infection. Eligible study designs comprised randomized controlled trials (RCTs), cohort studies, case–control studies, and cross-sectional studies. Only full-text articles published in English were considered. No restrictions were applied in terms of geographical location or healthcare setting. The primary objective of this review was to comprehensively characterize the clinical profile, severity spectrum, outcomes, and histopathological features of MAKI cases. Accordingly, studies that only reported the occurrence or incidence of renal involvement without providing detailed clinical characteristics, outcomes, or histopathological findings were excluded. Studies were also excluded if they were (i) review articles, editorials, letters to the editor, or conference abstracts; (ii) in vitro or animal studies; or (iii) publications in languages other than English or studies only including paediatric population.

Data sources and search strategy

A systematic search was done in PubMed/MEDLINE, EMBASE, and Cochrane CENTRAL to identify relevant studies published between January 1, 2000, and December 31, 2024. The search strategy included both Medical Subject Headings (MeSH) and free-text terms related to malaria and kidney injury, including: “Plasmodium,” “P. falciparum,” “P. vivax,” “P. knowlesi,” “malaria,” “acute kidney injury,” “kidney dysfunction,” “acute renal failure,” and “renal insufficiency.” The detailed search strategy for each database is provided in Supplementary Annex 1.

Study selection

Following the removal of duplicates, two independent reviewers (PM and VS) screened titles and abstracts for eligibility. Full texts of potentially eligible studies were assessed independently by two additional reviewers (AD and UK). Disagreements at any stage were resolved through discussion with a third reviewer (VK). In cases of multiple publications from the same study population, the most comprehensive dataset was selected. The complete study selection process is summarized in the PRISMA flow diagram (Fig. 1).

Fig. 1.

Prisma flowchart of the analysis

Data extraction

Data was collected using a standardized form developed a priori. Extracted variables included:

• Study characteristics: Author, year of publication, study setting, species of Plasmodium reported.

• Population details: Sample size, total number of malaria patients, number of patients with MAKI, age and sex

• Definitions: Criteria and classification systems used for AKI diagnosis

• Clinical presentation: laboratory parameters, AKI staging, dialysis requirement, mortality, and kidney histopathology (if available)

• Outcomes: follow-up duration, persistent kidney dysfunction, chronic kidney disease (CKD) development, and dialysis dependency at follow-up

Two reviewers conducted the initial data extraction independently. The extracted data were then verified by two additional reviewers to ensure accuracy and consistency.

Quality assessment

The methodological quality of the included studies was assessed using the Newcastle–Ottawa Scale (NOS) for observational studies [10]. Each study was evaluated across domains of selection, comparability, and outcome. The detailed quality assessment results are available in Supplementary Annex 2, Table 1. The certainty of the evidence across outcomes was evaluated using the GRADE (Grading of Recommendations Assessment, Development and Evaluation) framework. Two reviewers (PM and VS) independently performed the quality assessments; discrepancies were resolved through discussion and consensus.

Data synthesis

A descriptive synthesis of the included studies was conducted using Review Manager (RevMan) version 5.4 (Cochrane Collaboration, London, UK). Categorical variables were summarized as proportions and percentages for each clinical characteristic and outcome related to MAKI. A structured narrative synthesis approach was adopted to integrate and interpret findings across studies, for clinical presentation, kidney involvement and outcomes. A quantitative meta-analysis was conducted to estimate the pooled incidence of AKI and the pooled mortality among adult patients with MAKI. Studies were eligible for quantitative synthesis if they reported explicit numerators and denominators (the number of AKI cases and the total number of malaria cases for incidence, or the number of deaths and total AKI cases for mortality). Random-effects models (DerSimonian–Laird method) were used to account for inter-study heterogeneity. Proportions were stabilized using the Freeman–Tukey double-arcsine transformation and pooled with corresponding 95% confidence intervals. Statistical heterogeneity was quantified using I² index. Subgroup analyses were performed by Plasmodium species and geographic region. The publication bias was assessed visually using funnel plots and analytically with Egger’s regression test. All analyses were performed using random-effects models implemented in R, and results were summarized as forest plots showing individual study estimates, 95% confidence intervals, and pooled effects.

Results

Study characteristics

A total of 1,216 records were identified through initial database searches. After the removal of duplicates, titles and abstracts of the remaining articles were screened, resulting in the exclusion of 795 studies that were either unrelated to MAKI or lacked sufficient review relevance. Subsequently, 288 articles were excluded during full-text screening for the following reasons: 100 were case reports, 48 were review articles, 20 were not available in the English language, and 40 were conference abstracts with insufficient data. Additionally, one study was excluded due to the unavailability of its full text. A total of 25 studies [11–35] fulfilled the predefined inclusion criteria and were included in the final systematic review, of which 15 provided sufficient quantitative data for meta-analysis of AKI incidence and 23 for mortality analysis. These studies collectively reported on 2,094 patients diagnosed with MAKI. A detailed depiction of the study selection process is presented in Fig. 1 (PRISMA flowchart). Most studies were either prospective observational studies or retrospective analyses, with a few cross-sectional designs [14, 31]. All study settings were single-centre hospital-based design. The sample sizes ranged from small cohorts of 9 [20] to large datasets involving over 1191 patients [27]. While some studies focused exclusively on severe malaria cases [12, 13, 23, 25], others included broader populations of malaria patients with subsequent stratification based on kidney involvement.

Population characteristics

The characteristics of included studies, including design, geographic location, applied diagnostic criteria for AKI, species of Plasmodium involved, and mortality, are summarized in Table 1. The age range of the study populations varied widely, with most studies reporting mean ages in the 30 s and early 40 s. For instance, the mean age was 33.5 ± 17.2 years in the Pakistani cohort [12], 38.37 ± 15.08 years in an Indian cohort [34], and 27.7 ± 11.43 years in a Thai cohort [17]. A few studies included mixed populations comprising both adults and children, such as Umuhire et al. from Africa [35], though detailed stratification by age group was not consistently reported. Male patients constituted the majority in nearly all included studies, with reported proportions ranging from 60.5 to 89.3% where gender data were available.

Table 1.

Baseline study and population characteristics of the involved studies

	First author, year of publication	Country	Study design, setting	Species of malarial parasite involved, n (%)	Number of malaria cases, n (%)	Number of malaria cases with AKI n (%)	AKI definition used in the study	Mean age pf pts	Males, n (%)	Mortality n (%)
1	Mehta KS et al. 2001 [11]	India	Retrospective	P-Vivax: 3 (25) p-Falciparum- 16 (64) Mixed 5 (20)	402 (6.3%)	24 (5.97%)	S Cr > 1.5 mg/dl	21–40	19 (76)	7 (29)
2	Naqvi R et al. 2003 [12]	Pakistan	Prospective	P-Vivax:3 (2.4) p-Falciparum: 121 (97.5)	NR	124 (5.9%)	Serum creatinine > 2 mg/dl	33.5 ± 17.2	99 (80)	32 (26)
3	Maheshwari 2004 [13]	India	Prospective	P-Vivax: 2 (2.5) p-Falciparum:75(92.5) Mixed 4 (4.9)	NR	81	NR	35.5	70 (86.4%)	15 (18.5%)
4	Manan AJ et al. 2006 [14]	Pakistan	Cross-sectional	P -falciparum		46	WHO Criteria	32 ± 12.61	36 (78.26%)	11 (24%)
5	Mishra K et al. 2008 [15]	India	Prospective observational	P -falciparum	718	84 (11.8%)	Serum creatinine > 3 mg/dl	36	75 (89.3%)	44 (52.4%)
6	Kanodia KV et al., 2010 [16]	India	Retrospective	P -falciparum: 85 (85%,) P. vivax:2(2), and both in 13 (13%)	NR	100	Serum creatinine > 3 mg/dl	32 ± 12.61	63 (63%)	21 (21%)
7	Vannaphan S et al. 2010 [17]	Thailand	Prospective	P -falciparum	915	195 (21.3%)	WHO Criteria	27.7 ± 11.43	(78.5%)	12 (6.2%)
8	Tangpukdee N et al. 2011 [18]	Thailand	Prospective	p-Falciparum	189	63 (33.33%)	Serum creatinine > 3 mg/dl Oliguria	49 (77.7%)	128 (67.7%)	1 (15.8)
9	Krishna ChV et al. 2012 [19]	India	Prospective	P-Falciparum	NR	25	WHO Criteria	NR	NR	10 (40%)
10	Sinha A et al. 2012 [20]	India	Retrospective	P vivax	–	9	–	–	3 (33.3)	1 (11.1)
11	Kute et al. 2012 [21]	India	Prospective	P vivax	NR	202 malaria patients with AKI, Study only showed details of 25 (12.3%) by P. vivax	WHO Criteria	30.1 ± 12.3	NR	3 (12%)
12	Win KK et al. 2012 [22]	Thailand	Retrospective	p-Falciparum	262 cases of severe malaria	115 (44)	Serum creatinine (Cr) ≥ 3 mg/dl	31	190 (72.5)	56 (21.4)
13	Plewes K et al. 2014 [23]	Bangladesh	Retrospective	P falciparum	137 withsevere malaria	106 (77%)	Serum creatinine > 3 mg/dL	35	110 (80)	53 (39)
14	Kaushik R et al. 2013 [24]	India	Prospective	P. vivax monoinfection 195 (54.1) and174 (48.3) had P. falciparum	360	143 (39.7%) Only patients with P-vivax	RIFLE	41.59 + 18.17	26 (41)	6 (9.5%)
15	Shukla V et al. 2013 [25]	India	Prospective	P falciparum:73 (73.2%), P. vivax in 16 (15.8%), and mixed 12 (12%)	NR	101	Serum creatinine of ≥ 2 mg/dL, persisting for more than 24 h,	33.70 ± 15.39	76, (75.2)	10 (9.9)
16	Thanachartwet V et al. 2013 [26]	Thailand	Retrospective	P falciparum	257	190 (73.9)	RIFLE	31.0		36 (31.9)
17	Saravu K et al. 2014 [27]	India	Retrospective	P falciparum: 86 (58.9%), P. vivax in 56 (38.09%), and both in 15 (10.2%)	1,191	147 (12.3)	KDIGO	43.2 in mild AKI 38.9 in severe AKI	130 (88)	9 (6.1)
18	Nayak KC et al. 2014 [28]	India	Observational study	P falciparum:52 (27.22%, P. vivax: 14 (14.43%	288	66 (22.9)	WHO criterion	32.58 year	46 (70)	18 (27.27)
19	Koopmans et al. 2015 [29]	Netherlands	Retrospective	P falciparum	485, imported cases of malaria	39 (8%) of all patients and in 23 (38%) of the 61 patients with severe malaria	KDIGO	39	325 (73)	2 (5)
20	Naqvi R et al. 2015 [30]	Pakistan	Retrospective,	P vivax	–	671 developed AKI secondary to malaria of these 109 (1.93% of total AKI) patients had Vivax malaria	RIFLE	33.49 ± 14.67	66 (60.5%)	14 (12.84%)
21	Muhamedhussein MS et al. 2019 [31]	Tanzania	Cross-sectional study	P falciparum	104	27 (26)	KDIGO	38.65 ± 16.1	68 (65.5)	None
22	Kaur C et al. 2020 [32]	India	Retrospective case–control a	P. vivax: 5 (41.6%) P. knowlesi: 1 (8.3%) Mixed infections: 4 (33.3%)	NR	12	NR	NR	NR	NR
23	Anghan H et al. 2022 [33]	India	Prospective	P. vivax: 17 (47.2%) P. falciparum malaria: 19 (52.7%)	79 with severe malaria	36 (45.5)	AKI network (AKIN)	NR	NR	11/79 (13.9)
24	Naik H et al. 2023 [34]	India	Prospective	P-Vivax: 7 (3.46) Falciparum- 174 (86.14) Mixed 21 (10.39)	958	202 (4.7)	NR	38.37 ± 15.08	167 (82.6%)	11 (5.4)
25	Umuhire L et al. 2023 [35]	Rwanda	Reterospective	NR	122 cases with severe malaria	20 (16.2)	KDIGO	Both adult and peadiatric population included	63 (52.5)	3 (15%)

KDIGO Kidney Disease: Improving Global Outcome

WHO criteria: urine output < 400 mL/day, failure to improve after rehydration and/or rise in serum creatinine to greater than 3 mg/dL

RIFLE (Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease)

Geographical distribution of studies

The majority of studies were conducted in South Asia, with India contributing the highest number of publications (over 10 studies), followed by Pakistan and Thailand. This regional predominance reflects the high endemicity of malaria and the substantial burden of Plasmodium falciparum and P. vivax in these countries. From Thailand some prospective studies [17, 18, 26] were published. Tanzania [31] and Rwanda [35] contributed limited but important data from Sub-Saharan Africa a region with a high incidence of severe malaria but fewer AKI-focused publications. Majority of the studies published from this region were on paediatric population, thus excluded from the review. One study from the Netherlands by Koopmans et al. [29] highlighted MAKI in non-endemic settings, specifically among imported cases in travellers.

Species of Plasmodium involved

Plasmodium falciparum was the predominant species implicated in AKI across nearly all studies. Monoinfection with P. falciparum accounted for over 80% of cases in several studies [12, 14, 17, 23]. Mixed infections with P. vivax and P. falciparum were reported in studies from India [11, 27, 33], reflecting endemic co-circulation. Studies from the Indian cohorts by Kaushik et al. [24] and Kute et al. [21], as well as the Pakistani cohort by Naqvi et al. [30], reported outcomes exclusively caused by P. vivax–associated AKI. Rare species such as P. knowlesi were also reported in isolated cases [32].

AKI criteria used

Definitions of AKI varied significantly among the studies. Early investigations tended to use absolute serum creatinine thresholds, such as > 1.5 mg/dL [11], > 2 mg/dL [12, 25]. In contrast, more recent studies applied standardized classification systems including the RIFLE [24, 30], KDIGO [27, 31], and AKIN criteria [33]. The WHO criteria remained widely used across studies from Southeast Asia and South Asia [14, 17, 19]. Most studies relied on serum creatinine measurements alone; only a few incorporated urine output or oliguria into the diagnostic process [18].

Kidney Involvement: Kidney manifestations among malaria patients varied significantly in presentation and severity (Table 2). The proportion of malaria cases complicated by AKI ranged from 2.4 to 45.5%. The pooled incidence of AKI among adults patients with malaria was 26.5% (95% CI 19.8–34.4; I² = 97%), with considerable heterogeneity most likely attributable to differences in AKI definitions and Plasmodium species (see supplementary Fig. S1). Funnel plot assessing publication bias for AKI incidence in provided in Fig. S2. Higher incidence was reported in more recent prospective studies: Anaghan et al. from India [33] observed AKI in 44% of severe malaria cases, while Plewes et al. from Bangladesh [23] reported a 77% incidence among patients with severe malaria requiring ICU. The impact of AKI definition criteria was evident: studies applying standardized classifications (RIFLE, AKIN, KDIGO) reported higher and more precise incidence estimates (31%) than those using non-standard thresholds (23%), emphasizing the need for uniform diagnostic approaches. The pooled incidence was highest among P. falciparum infections (34%, 95% CI 28–41) and intermediate in mixed-species infections (28%, 95% CI 20–37), whereas cohorts with P. vivax monoinfection showed a incidence of (21%, 95% CI 16–28). Isolated P. knowlesi cases were reported only sporadically and were not suitable for pooled analysis. Regional subgrouping also showed clear geographic differences. Studies from Southeast Asia (Thailand, Bangladesh) reported the highest pooled incidence (33%, 95% CI 25–42), followed by South Asia (India, Pakistan) at 29% (95% CI 24–35). African cohorts (Tanzania, Rwanda) yielded an overall incidence of 21% (95% CI 15–29), which represents the weighted mean of the two available studies rather than a true meta-analytic estimate. Imported malaria cases from Europe (Netherlands) showed a markedly lower AKI frequency (8%) and were analysed descriptively. See Supplementary Table 2 for subgroup analysis of AKI incidence among adults with malaria as per Plasmodium species and geographical region. Oliguria was the most commonly reported feature, present in up to 82% of patients in studies such as Kanodia et al. [16] and Naqvi et al. [12], with others reporting rates ranging from 24.2% [28] to 76.1% [14]. Haematuria and proteinuria were also documented, albeit less consistently. AKI staging was inconsistently reported across studies. Among those applying staging, severe AKI was frequently encountered; Mehta et al. [11] reported that 75% of cases had creatinine > 8 mg/dL, while Plewes et al. [23] categorized over 23% of patients as having severe AKI. Mean serum creatinine at presentation ranged widely, from 1.53 mg/dL [23] to over 10.9 mg/dL [11, 12], reflecting both heterogeneity in disease severity and healthcare access. Dialysis requirements were substantial in many cohorts.

Table 2.

Kidney involvement in patients with malaria

Author with year of publication	Oliguria, n (%)	Hematuria n (%)	Proteinuria n (%)	AKI staging n (%)	Dialysis requirement n (%)	Mean creatinine mg/dL	Electrolyte imbalance n (%)
Mehta KS et al. 2001 [11]	10 (40)	3 (12)	3 (12)	18 (75%) had severe AKI (S.cr > 8 mg/dl)	22 (92)	10.3 ± 5.8	NR
Navi R et al. 2003 [12]	84 (68)	53 (43)	42 (33.8)	NR	99 (79.8)	9.4 ± 5.39	Hyperkaemia:125 (20), Hyponatremia: 56 (45)
Maheswari A et al. 2004 [13]	33 (41)	48 (59.3)	15 (18.5)	NR	35 (43.2)	NR	Hyponatraemia: 58.19%, hyperkalaemia 33.8%, hypematraemia 5.4% and hypokalaema 2.7%
Manan AJ et al. 2006 [14]	35 (76.09)	10 (21.74)	13 (28.26)	NR	36 (78.26)	6.29 ± 2.48	Hyponatremia: 13 (28.2)
Mishra S et al. 2008 [15]	47 (56.0)	NR	NR	NR	NR	NR	Hyponatremia: 16 (24%); hypokalaema8 (9.5%)
Kanodia KV et al. 2010 [16]	82 (82)	44 (44)	38 (38)	NR	78 (78)	9.2 ± 4.2	Hyperkalaemia 26 (26%) Hyponatremia (< 130 meq/L) 32 (32%)
Vannaphan S et al. 2010 [17]	NR	NR	NR	NR	171 (87.7)	NR	Hyponatremia: 162 (84%) had Hypernatremia 2 (1%), Hypokalemia: 52 (27%), Hyperkalemia: 17 (9%)
Tangpukdee N et al. 2011 [18]	NR	NR	NR	NR	46 (73)	3.7	NR
Krishna ChV et al. 2012 [19]	18 (72)	NR	4 (16)	NR	20 (80)	NR	Hyponatremia: 16 (64%)
Kute et al. 2012 [21]	NR	NR	NR	NR	100%	7.37 ± 2.6	NR
Win KK et al. 2012 [22]	79 (49.4)	51 (44.3)	NR	NR	53 (46.1)	1.8 (1.2–4.1)	NR
Plewes K et al. 2014 [23]	NR	NR	NR	Mild, moderate and severe AKI in 32 (23), 42 (31) and 32 (23) respectively	39 (28%) required but only 19 received	1.53 (1.37–1.73)	NR
Kaushik R et al. 2013 [24]	30 (48)	None	7 (11)	RIFLE class: R, class I and class F in 27 (43%), 23 (37%) and 13 (21%) patients, respectively	14 (22.2)	4.1 + 3.04	Hyperkalaemia: 9 (14), Hypernatraemia: 5 (8),Hyponatraemia: 3 (5)
Shukla V et al. 2013 [25]	45 (44.5)	NR	NR	NR	37 (36.6%)	4.09 2.98	NR
Thanachartwet V et al. 2013 [26]	NR	NR	NR	R (40/257, 15.6%), RIFLE-I (43/257, 16.7%), and RIFLE-F (107/257, 41.6%)	53 (27.8), but 45.2% of severe P falciparum malaria patients with AKI required dialysis	1.8 (1.2–4.1) mg/dL	NR
Saravu K et al. 2014 [27]	NR	17 (11.5)	67 (45.5)	Mild AKI: 101 (12.26%) Severe AKI: 46 (5.58%)	NR	Mild AKI group: 1.8 [1.6, 2.2] Severe AKI: 5.2 [4.2, 7.8]	NR
Nayak KC et al. 2014 [28]	16 (24.2)	24 (36.3)	31 (47)	NR	7 (10.6)	3.87 ± 1.07	NR
Sinha A et al. 2015 [20]	NR	NR	NR	NR	9 (100)	7.9	NR
Koopmans LC et al. 2015 [29]	NR	NR	NR	KDIGO stage 1: 12 (30.7), stage 2: 8 (20.5), stage 3:7 (17.9)	8 (20.5)	1.8	NR
Navi R et al. 2015 [30]	76 (69.72)	61 (81.33)	43 (57.33)	NR	82 (75.22%),	10.01 + 4.44	Hyperkaemia:14 (12.84) Hyponatremia: 27 (24.77)
Muhamedhussein MS et al. 2019 [31]	NR	39 (38.2)	72 (69.2)	NR	2 (19)	1.63	NR
Kaur C et al. 2020 [32]	9 (75)	1 (8.3)	6 (50)	NR	NR	6.1	NR
Anghan H et al. 2022 [33]	NR	NR	NR	Stage 1:9 (25), Stage 2: 8 (22) and Stage 3:19 (53%)	20 (55.5)	NR	NR
Naik H et al. 2023 [34]	137 (67.82)	61 (30.2)	132 (65.35)	NR	N = 152 (75.75) Hemodialysis: 82.12% Peritoneal dialysis: 17.88%	NR	Hyponatremia: 123 (60.89)
Umuhire L et al. 2023 [35]	NR	NR	NR	NR	6 (30)	NR	NR

KDIGO Kidney Disease: Improving Global Outcome, Scr Serum creatinine, AKI Acute kidney injury, NR Not reported, RIFLE Risk, Injury, Failure, Loss of kidney function, and End-stage kidney disease

Proteinuria considered positive if Dipstick protein > 1 + (30 mg/dL)

Rates ranged from 20.5% [29] to over 90% [12, 21] Notably, in Naik et al. [34], 75.8% of patients required dialysis, with 82% undergoing haemodialysis and 18% receiving peritoneal dialysis. Resource limitations were evident in Plewes et al. from Bangladesh [23], where 39 patients required dialysis but only 19 received it. Electrolyte imbalances were frequently documented, with hyponatraemia emerging as the most common abnormality. Studies such as Vannaphan et al. [17] and Naik et al. [34] reported hyponatraemia in over 60% of patients. Hyperkalaemia was also observed, particularly in studies involving severe AKI [12, 16]. Saravu et al. reported icterus and hepatomegaly as independent predictors of AKI [27]. Manan noted that among AKI patients, 89.13% had thrombocytopenia, 28.26% hyponatraemia, 19.57% cerebral malaria, and 19.57% metabolic acidosis [14]. Tangpukdee et al. found oliguria in the first 24 h and prior residence in a non-endemic area to be independent predictors of AKI [18]. Some studies have identified factors associated with MAKI including high parasitaemia, hyperbilirubinaemia, volume depletion, a hypercatabolic state, intravascular haemolysis, sepsis and hypoglycaemia [21, 25, 33]. Plewes et al. associated elevated bilirubin, high lactate levels, and low bicarbonate with worsening AKI [23].

Differences in AKI characteristics by malaria species

Plasmodium falciparum remained the leading cause of AKI, associated with higher rates of severe AKI, need for dialysis, and mortality [12, 27]. Saravu et al. showed that AKI patients with P. falciparum had higher rates of anaemia, jaundice, and hepatomegaly, while P. vivax patients exhibited significant splenomegaly and tachycardia [27] with increasing AKI severity (p < 0.001 for both heart rate and splenomegaly). In a study by Anaghan et al., patients with P. falciparum–associated AKI were more likely to require dialysis compared to those with P. vivax–associated AKI, a difference that was statistically significant (p = 0.02) [33]. Additionally, acidosis, sepsis, and kidney failure were more commonly observed in P. falciparum infections than in P. vivax malaria. However, P. vivax monoinfection was associated with increased reports of thrombotic microangiopathy (TMA), acute cortical necrosis (ACN), and sometimes equivalent severity of AKI as P. falciparum malaria [20, 21]. Plasmodium knowlesi was also reported, albeit infrequently. In the study by Kaur et al. from India among twelve malaria patients with AKI, one case was attributed to P. knowlesi infection [32]. While detailed clinical outcomes specific to the P. knowlesi case were not provided, its inclusion is clinically significant given the distinct pathogenic mechanisms associated with this zoonotic parasite. Unlike P. falciparum, where cytoadherence and microvascular sequestration predominate, AKI in P. knowlesi infection appears to result primarily from intravascular haemolysis, microvascular dysfunction, and endothelial activation [36].

Mortality outcomes

Mortality rates among patients with MAKI varied widely across the included studies, ranging from 5 to over 52% (Table 1). The pooled mortality among adults MAKI patients was 19.2% (95% CI 12.9–27.7%), with substantial between-study heterogeneity (I² = 92%) (see Fig. S3).

When stratified by species, the highest fatality was observed among P. falciparum infections (19%, 95% CI 14–25), followed by mixed-species cohorts (15%, 95% CI 10–22) and P. vivax infections (11%, 95% CI 7–17). Mortality among P. knowlesi infections was rarely reported and insufficient for quantitative pooling. Studies from Southeast Asia exhibited the highest pooled mortality (20%, 95% CI 14–27), followed by South Asia (16%, 95% CI 11–22). In contrast, studies from Africa reported substantially lower mortality (9%, 95% CI 5–15), while imported malaria cases from Europe demonstrated mortality of around 5%. See supplementary Table 3 for Subgroup analysis of mortality among adults with MAKI. Funnel plot assessing publication bias for mortality in provided in Fig. S4. Mishra et al. reported one of the highest mortality rates at 52% in an Indian cohort [15]. Other important reports include Plewes et al. from Bangladesh [23], Naqvi et al. [12] and Manan et al. from Pakistan [14], with mortality rates of 39%, 26%, and 24%, respectively. In contrast, more recent studies, such as that by Naik et al. [34], showed improved outcomes with a markedly lower mortality rate of 5.4%. Mortality correlated with AKI severity. Saravu et al. showed 0.3%, 2%, and 15.2% mortality in no/mild/severe AKI categories [27]. Kaushik et al. found 3.7%, 4.3%, and 30.7% mortality for RIFLE Risk/Injury/Failure categories respectively [24]. Key predictors included delayed diagnosis, anaemia, shock, acute respiratory distress Syndrome (ARDS), need for ventilation, raised transaminases, and metabolic acidosis.

Naik et al. listed causes of death as multiorgan dysfunction, status epilepticus, disseminated intravascular coagulation (DIC), fractured renal cast and ARDS with gastrointestinal bleeding [34]. Krishna et al. showed lower survival in patients with delayed hospital presentation (p = 0.014) [19]. Naqvi et al. also reported presence of jaundice, thrombocytopenia, central nervous system involvement, mechanical ventilation requirement and haematuria as the factors significantly associated with high mortality [30]

Follow up and long-term kidney sequelae

Long-term follow-up data on MAKI remain limited, with durations ranging from 3 weeks to 3 months as reported in selected studies. Despite the heterogeneity in study designs and populations, complete kidney recovery was the most frequently observed outcome (Table 3). In a study by Naqvi et al. among 109 patients with Plasmodium vivax–associated MAKI, complete recovery was noted in 69 patients (63.3%), partial recovery in 22 (20.2%), and 3 patients progressed to kidney failure [30]. Similarly, in a case series of 25 patients with P. vivax–associated MAKI, 3 (12%) patients showed persistent renal dysfunction (serum creatinine 1.5–3 mg/dL) at follow-up [21]. Kanodia et al. reported that, among 100 patients with MAKI, 10 (10%) had residual renal dysfunction (serum creatinine 1–3 mg/dL), and 5 (5%) remained dialysis-dependent [16]. In the series by Koopman et al. among 39 cases of imported P. falciparum malaria, five of the eight (63%) patients who required KRT recovered renal function during hospitalization, while two progressed to kidney failure [29]. Sinha et al. [20] evaluated nine patients with TMA and MAKI following P. vivax malaria; all required haemodialysis, and six remained dialysis-dependent at 4 weeks. (Additionally, Krishna et al. reported the development of CKD in one patient 3 months post-P. vivax malaria [19]. Sinha et al. [20] reported that delayed presentation, haemolysis, and prolonged oligoanuria significantly predicted dialysis dependency. Risk factors for poor outcomes included older age, delayed hospitalization, jaundice, ARDS, and cerebral malaria [11, 12, 25, 33].

Table 3.

Follow up and outcome of malaria-associated AKI

Author	Follow up duration	CKD development N (%)	Dialysis dependency, n (%)
Mehta KS et al. [11]	6 weeks	0/17	0/17
Naqvi R et al. [20]	NR	0/77	0/77
Maheswari et al. [13]	Till death or recovery of renal function	0/66	0/66
Manan AJ et al. [14]	NR	0/35	0/35
Kanodia KV et al. [16]	NR	10 /79 (10)	5/79 (5)
Naqvi R et al. [30]	NR	23/95 (20.18)	3/95 (3)
Kute et al. [21]	3 weeks	3/25 (12)	0/25
Krishna ChV et al. [19]	3 months	1/25 (4)	None
Kaushik R et al. [24]	NR	0/57	0/57
Shukla V et al. [25]	3 months	None	None
Nayak KC et al. [28]	3 weeks	0/48	0/48
Sinha A et al. [20]	4 weeks	0/9	6/9 (66.6)
Koopmans LC et al. [29]	NR	0/39	2/39 (5)
Naik H et al. [34]	4 weeks	0/191	0/191

NR Not reported, CKD chronic kidney diseases

Histopathological spectrum in MAKI

Kidney histopathology was available in 95 biopsy-confirmed cases of MAKI across 10 studies included in this review (Table 4). The most prevalent lesion was acute tubular necrosis (ATN), observed in 43 patients (45.3%), with several studies noting the presence of pigmented casts, suggestive of haem-mediated tubular injury secondary to intravascular haemolysis or rhabdomyolysis. Naik et al. [34] reported ATN in 50% of their cohort, with severe forms characterized by pigmented and red blood cell casts. ACN was the second most frequently reported lesion, seen in 20 cases (21%), with the highest prevalence in the series by Kaur et al. [32], where ACN was identified in 50% of biopsies. TMA was described in 13 cases (13.7%), most notably in the study by Sinha et al. [20], where all nine biopsied patients demonstrated TMA, often in conjunction with tubulointerstitial nephritis (TIN) or ACN. Membranoproliferative glomerulonephritis (MPGN), often lacking immune complex deposition, was reported in 17 patients (17.9%), with Nayak KC et al. [28] contributing the largest subset (12/18), frequently coexisting with ATN. Less common histological entities included collapsing glomerulopathy [29], crescentic glomerulonephritis [30], membranous nephropathy [16], and mesangial IgA deposition [34], reflecting the broad pathological heterogeneity of MAKI, involving tubular, glomerular, vascular, and interstitial compartments. However, several important caveats must be acknowledged. The timing of kidney biopsy was not uniformly reported across studies and likely reflects a selection bias toward patients with delayed or incomplete renal recovery. Furthermore, clinical correlations linking specific histopathological lesions to demographic or biochemical profiles were not described. Despite these limitations, the presence of severe vascular lesions such as TMA and can particularly in studies by Sinha et al. [20], Kanodia et al. [16] Kute et al. [21] and Naqvi et al. [30] was often associated with poor renal outcomes, including progression to CKD or kidney failure. In particular, TMA lesions have been increasingly recognized in Plasmodium vivax-associated AKI [20, 21]. Chakrabarti et al. [37] reported three cases of P. vivax-associated TMA, with two patients progressing to kidney failure, and one achieving full renal recovery. These findings highlights the potential for irreversible kidney injury in P. vivax-associated MAKI, particularly in the presence of cortical necrosis or TMA. In a study by Amoura et al. [38]. 23 patients with imported malaria were evaluated, including 10 with concomitant HIV infection; all were recent travellers to France from endemic regions. Plasmodium falciparum was identified in 22 cases, and P. malariae in one. Nephrotic syndrome was diagnosed in 17 patients; kidney biopsies revealed focal segmental glomerulosclerosis (FSGS) in 21, 18 of which were collapsing variants, including 9 cases of HIV-associated nephropathy and minimal change disease in 2 cases [39]. Immunohistochemistry detected P. falciparum histidine-rich protein-2 in tubular cells of 4 patients, but not in podocytes or parietal epithelial cells. All 7 patients tested harboured high-risk APOL1 genotypes. Over a 23-month mean follow-up, 8 patients required KRT, and the remaining had a mean eGFR of 51 mL/min/1.73 m². Figure 2 provides a visual graphic of the key findings from this study.

Table 4.

Histopathological spectrum in malaria-associated AKI

Author	Kidney biopsy findings, n %
Mehta KS et al. [11]	n = 5/17 (29.4%). All cases showed ATN with pigmented cast and mesangial proliferation
Kanodia KV et al. [16]	n = 10/79 (10%), Patchy cortical necrosis 7 (70%), MPGN without any immune deposits, and ATN (20%) and membranous GN 1 (10%)
Sinha A et al. [20]	n = 9/9 (100%) TMA with variable TIN and ATN or ACN
Kute et al. [21]	n = 4/25 (16%), Patchy cortical necrosis, n = 3, and ATN-n = 1
Kaushik R et al. [24]	n = 2/57. Changes of ATN and MPGN any immune deposits were seen in one patient, and ATN in the other
Nayak KC et al. [28]	n = 18/48 (37.2%), MPGN: 12/18 cases. Two cases had isolated MPGN while it was seen along with changes of ATN in 10 cases
Koopmans LC et al. [29]	n = 2/39, Severe ischemic changes and TIN with advanced scarring (n = 1) and collapsing glomerulopathy (n = 1)
Naqvi R et al. [30]	n = 15/95 (13.7%), ATN: 6 (40%), ACN: 4 (26%), TIN: 2 (13%), and Crescentic GN: 2 (13%)
Kaur C et al. [32]	n = 12/12 (100%), ATN: 3 (25%), ACN: 6 (50%), and TMA: 4 (33.3%)
Naik H et al. [34]	n = 18/191 (9.4%), ATN 9 (50%), Severe ATN with pigmented casts: 2 (11.33%), Severe ATN with pigmented casts and RBC casts: 1 (5.5%), Focal glomerular dilatation: 2 (11.33%) and Mesangial IgA deposition: 1 (6.67%)

MPGN Membranoproliferative glomerulonephritis (GN), ATN acute tubular necrosis, ACN Acute cortical necrosis, TMA Thrombotic microangiopathy, RBC Red blood cells, TIN Tubulointerstitial nephritis

Fig. 2.

Visual graphic summarizing the key findings of the study

Discussion

This systematic review and metaanalysis comprehensively synthesizes data from 25 studies encompassing over 2,000 patients with MAKI providing critical insight into its epidemiology, clinical profile, and outcomes. The findings emphasize on the growing recognition of kidney complications in malaria, particularly in endemic regions. Geographically, the highest volume of studies originated from South Asia particularly India, which accounted for nearly half of the included studies followed by Pakistan and Thailand. In this region, both P. falciparum and P. vivax circulate widely, often in mixed infections. Several Indian studies demonstrated P. vivax-related AKI with severity comparable to P. falciparum, contradicting earlier assumptions about its benignity. Sinha et al. and Kute et al. from India reported biopsy-proven TMA and ACN, and persistent dialysis dependency in patients with P. vivax monoinfection, suggesting a vasculopathic phenotype that may be underrecognized in endemic settings [20, 21]. In contrast, studies from Thailand and Bangladesh focused almost exclusively on P. falciparum, with reported AKI rates as high as 77% in severe malaria cohorts and dialysis requirements exceeding 70% in certain groups. Key findings include the wide variability in AKI incidence, severity, and dialysis requirement, as well as heterogeneity in diagnostic criteria and follow-up duration. Despite the diversity of study designs and settings, a few common threads emerge: AKI in malaria is frequently severe, often necessitates KRT and is associated with substantial mortality, particularly in resource-constrained environments. An important observation is the inconsistent application of AKI definitions across studies, ranging from crude creatinine cut-offs to more structured classifications, such as RIFLE, AKIN, and KDIGO. This methodological variability impedes comparability across studies and may lead to under- or overestimation of AKI prevalence. Moreover, only a minority of studies incorporated urine output into the diagnostic criteria, despite its critical role in AKI assessment. This highlights a missed opportunity when the important tool of urine output is not utilized by clinicians and possible underreporting of MAKI cases.

The clinical spectrum of MAKI is diverse, with oliguria, haematuria, and proteinuria emerging as consistent features, though their documentation remains patchy. Severe AKI, defined by marked elevations in serum creatinine or need for dialysis, was common reported in up to 75% of patients in several studies with dialysis rates exceeding 90% in some cohorts.

The clinical and pathological diversity observed across the included studies reflects not only biological differences in Plasmodium species but also disparities in healthcare infrastructure and diagnostic capabilities across endemic regions. Sub-Saharan Africa, despite bearing the world’s highest malaria burden, was underrepresented, with only two eligible studies from Rwanda and Tanzania [31, 35]. This paucity of data is concerning and highlights a critical gap in the global MAKI literature, particularly for adults. The available African studies did show P. falciparum predominance and documented MAKI rates between 16 and 26%, but long-term outcomes were not reported. This regional gap likely reflects both logistical barriers to nephrology research and the prioritization of paediatric malaria studies, many of which were excluded in this adult-focused review. Moreover, differences in healthcare infrastructure profoundly affect outcomes. For example, in Bangladesh, despite 39 patients requiring dialysis, only 19 received it due to resource constraints an outcome that would be rare in high-income settings. Similarly, delayed presentation, which was consistently associated with higher mortality and persistent renal dysfunction in India and Pakistan, underscores the need for earlier AKI recognition and referral pathways. The single European study [29] on imported malaria offers a stark contrast demonstrating early diagnosis, aggressive supportive care, and a mortality rate of just 5%, despite including severe cases.

The review showed that oliguric AKI was the predominant clinical manifestation, present in up to 80% of cases in multiple cohorts with proteinuria and haematuria were inconsistently reported suggesting glomerular as well as tubular injury.

MAKI results from a complex interplay of parasite-induced, immune-mediated, and microvascular mechanisms (Fig. 3). Plasmodium falciparum is most commonly implicated due to its unique ability to cause cytoadherence and sequestration of infected erythrocytes in renal microvasculature, leading to vascular congestion, hypoperfusion, and ischemic tubular injury. Haemolysis and intravascular haemoglobin release contribute to pigment nephropathy, while immune activation results in cytokine storms and endothelial dysfunction, further exacerbating renal insult. Inflammatory mediators, such as TNF and IL-6, increase vascular permeability and contribute to tubular necrosis [2, 4, 38].

Fig. 3.

Mechanism of malaria associated AKI

Additionally, volume depletion, shock, and bleeding are common in severe malaria and precipitate pre-renal AKI. Plasmodium knowlesi has also rapidly emerged across Southeast Asia as a major cause of severe malaria in humans, particularly in Malaysia and surrounding regions. Early series from Sabah, Malaysia, reported AKI in up to 55% of severe P. knowlesi cases, with high case-fatality rates showing its virulence and the propensity for multiorgan dysfunction [40]. Subsequent large cohort analyses demonstrated that severe P. knowlesi frequently presents with intravascular haemolysis, endothelial activation, and microvascular dysfunction, mechanisms strongly linked to AKI pathogenesis [36]. Barber and colleagues further showed that circulating free haemoglobin levels were markedly elevated in P. knowlesi malaria and independently associated with microvascular injury markers, elevated serum lactate, and worsening kidney function [36]. These findings support the concept that endothelial injury and haemolysis-mediated oxidative stress, rather than parasite sequestration (as in P. falciparum), are the primary drivers of renal dysfunction in P. knowlesi malaria. Furthermore, the PACKNOW randomized controlled trial evaluated acetaminophen as a nephroprotective adjunct for haemolysis-related kidney injury in severe P. knowlesi malaria, highlighting ongoing translational efforts to mitigate renal complications [41]. Consistent with these data, regional surveillance from Malaysian identified P. knowlesi as the dominant malaria species in several districts, with renal failure and metabolic acidosis frequently reported among fatal cases [42].

The review also offers novel insights into the histopathological landscape of MAKI. Among 95 biopsy-proven cases, ATN emerged as the dominant lesion, often with pigmented casts indicative of haem-mediated tubular injury. However, more ominous vascular lesions like ACN and TMA were not uncommon, particularly in P. vivax infections. This contradicts the classical paradigm that reserves vascular injury for falciparum malaria. Furthermore, the detection of MPGN and crescentic GN in several biopsies expands the spectrum of malaria-related glomerular pathology. Additionally, the presence of collapsing glomerulopathy and crescentic GN in imported malaria cases from non-endemic countries such as the Netherlands points to the potential role of host susceptibility. Yet, histopathology data were limited by selection bias as biopsies were often performed only in non-resolving or dialysis-dependent cases and lacked temporal correlation with clinical events. Future prospective cohorts with protocolized biopsy timing are necessary to elucidate histological predictors of recovery or progression to CKD.

Mortality outcomes varied widely across the included studies, from as low as 5.4% to as high as 52% in older reports. This variability is partly attributable to differences in AKI severity, species, and supportive care access. Long-term follow-up data were disappointingly sparse, with most studies restricted to a few weeks of observation. Nevertheless, the limited available data suggest a predominance of full renal recovery, although partial recovery and progression to kidney failure were not uncommon. Critically, no study tracked long-term eGFR decline, albuminuria, or progression to kidney failure. This leaves a large blind spot in the understanding of the true burden of malaria-associated CKD, especially in populations repeatedly exposed to malarial infections. In a questionnaire based study from Sri Lanka, dehydration, history of malaria and drinking untreated well water from were reported to be likely contributors to the development of CKD of unknown aetiology [43].

This review is strengthened by its robust methodology, broad geographic coverage, and inclusion of histopathological data, offering a rare multidimensional perspective on MAKI. It highlights regional variability in species distribution, disease severity, and outcomes, thereby emphasizing the need for localized management strategies. Nonetheless, the review is constrained by several limitations. The observational nature of all included studies limits causality assessment. Studies heterogeneities particularly in AKI definitions and outcome reporting precluded quantitative synthesis. Furthermore, the underrepresentation of African and Latin American data limits the generalizability of findings, especially given the high malaria burden in those regions. Studies exclusively involving paediatric populations was excluded from the analysis. Obeagu et al. conducted a systematic review on AKI in severe malaria, highlighting the heightened vulnerability of children to both AKI and associated mortality in severe malaria [44]. The type of dialysis modality, whether haemodialysis or peritoneal dialysis was seldom specified in detail, with few studies analysing the impact of dialysis timing or frequency on mortality and renal recovery. This points to a major evidence gap in optimizing RRT strategies in MAKI, especially in low-resource environments.

Future research must focus on several fronts. First, standardized definitions and reporting protocols ideally anchored in KDIGO and ISN 0by25 frameworks should be adopted to improve data comparability. Second, species-specific prospective studies are needed to elucidate pathophysiological mechanisms, particularly the vascular injury signature of P. vivax and P. knowlesi species. Third, nephrology surveillance programs should be integrated into malaria control efforts to capture long-term outcomes, especially CKD progression. Finally, equitable dialysis access remains a moral and logistical imperative in endemic LMICs. By aligning infectious disease management with renal care infrastructure, we can improve both survival and long-term quality of life for patients with MAKI a neglected yet devastating complication of one of the world’s most ancient diseases. Search of biomarkers for early detection and risk stratification of survivors is imperative. Randomized implementation studies are needed to assess the impact of early dialysis, tele-nephrology, and mobile RRT units in rural or resource-limited regions.

Conclusion

MAKI is a clinically significant yet underrecognized complication, with regional variability in causative species, severity, and outcomes. Plasmodium falciparum predominates globally, but P. vivax is increasingly linked to severe renal pathology. Mortality and dialysis needs remain high, especially in low-resource settings. Long-term follow-up reveals that while many patients recover, a small subset progresses to CKD or kidney failure. Standardized diagnostic criteria, prospective species-specific studies, and improved access to kidney support are essential to mitigate the burden of MAKI and align with global AKI reduction goals.

Abbreviations

ATN

Acute tubular necrosis

MAKI

Malaria-acute kidney injury

ACN

Acute cortical necrosis

AKI

Acute kidney injury

CKD

Chronic kidney disease

ESKD

End-stage kidney disease

KDIGO

Kidney disease: improving global outcomes

TMA

Thrombotic microangiopathy

RRT

Renal replacement therapy

TMA

Thrombotic microangiopathy

Author contributions

PM conceptualized the idea and drafted the manuscript. VS, EM, and UK collected the data. VK verified the data. RK reviewed and edited the manuscript. PM interpreted the data and edited the manuscript.

Funding

None.

Data availability

The datasets used and/or analysed during the current study available from the corresponding author on reasonable request.

Declarations

Ethics approval and consent to participate

Not applicable.

Consent for publication

Not applicable.

Competing interests

The authors declare no competing interests.