Abstract
We report the case of a 75-year-old woman with steroid-resistant minimal change disease (MCD) whose refractory proteinuria and hypoproteinemia were controlled with early low-density lipoprotein apheresis (LDL-A). She was initially treated with steroid therapy, including methylprednisolone pulse. However, her hypoproteinemia, severe proteinuria, accompanied with renal insufficiency persisted despite these therapies. We initiated hemodialysis on day 17, and LDL-A on day 18. After the treatment, we found an improvement in her urine protein excretion, hyperlipidemia, and hypoproteinemia gradually. Her renal function returned to normal. We added cyclosporine A (CyA) after confirming the normal renal function. Her proteinuria was 0.693 g/day on day 350 and she achieved incomplete remission type I. There are few reports of the efficacy of LDL-A in older patients with MCD with acute kidney injury (AKI). In addition, there are only a few reports of cases in which LDL-A was introduced early, as in this case. This case suggests that early LDL-A may be an effective therapy for steroid-resistant MCD with AKI.
Keywords: Minimal change disease, Low-density lipoprotein apheresis, Acute kidney injury, Hemodialysis, Nephrotic syndrome
Introduction
Minimal change disease (MCD) is a major cause of idiopathic nephrotic syndrome (NS), characterized by intense proteinuria leading to edema and intravascular volume depletion. It occurs not only in children but also in adults, including those over the age of 60 [1–3]. Very elderly patients (aged ≥ 75 years) with MCD may take a longer time to achieve complete remission compared to elderly patients (aged 65–74 years) [1]. Although the glomeruli appear normal on light microscopy in MCD at the time of presentation, some cases show a modest reduction in glomerular filtration rate (GFR). Acute kidney injury (AKI) with MCD is due to the impairment of water and solute filtration function caused by foot process effacement [2]. In adults, whose renal reserve is lower than that of children, there are reports that patients with older age, hypertension, more severe hypoalbuminemia and proteinuria were more likely to develop AKI and were resistant to steroids [3]. Heavy persistent proteinuria is a risk factor for end-stage renal disease, as well as significant morbidity and mortality associated with thrombotic and cardiovascular complications [4].
Most NS patients are empirically treated with corticosteroids. Many achieve remission with favorable outcomes, as steroid-responsive MCD typically dose not progress to chronic kidney disease. However, some cases are steroid-resistant. Low-density lipoprotein apheresis (LDL-A) is a key therapy for such cases. It has been used in clinical practice for the treatment of renal disease with steroid-resistant NS, specifically focal segmental glomerulosclerosis (FSGS) [5]. Furthermore, patients with NS caused by non-FSGS such as MCD were also found that LDL-A reduced the urine protein level at a comparable rate to that in FSGS cases immediately after the treatment [6]. However, the appropriate timing for initiating LDL-A is still a topic of debate. We hypothesized that early initiation of LDL-A could improve AKI and severe proteinuria caused by MCD and help discontinuation of hemodialysis even in elderly patient. We report a case of an elderly woman who suffered from steroid-resistant MCD and needed hemodialysis due to AKI, effectively treated with early LDL-A.
Case presentation
A 75-year-old woman was referred to our hospital with symptoms of general fatigue and edema in her legs. She had no past medical history and no medication. She had no allergy to food or medication. An examination revealed the following: height 154 cm, weight 54.6 kg, blood pressure of 159/103 mmHg, heart rate of 81 beats/min, respiratory rate of 18/min, and SpO2 saturation of 98%; room air. The laboratory investigations (Table 1) revealed severe proteinuria (15.506 g/gCr) with hematuria, hypoproteinemia, and hyperlipidemia. Her renal function was normal. Serum immunofixation electrophoresis and urinary immunoelectrophoresis revealed no monoclonal immunoglobulin and Bence Jones’ protein, respectively. The proteinuria selectivity index was 0.09. Computed Tomography showed bilateral renal slight enlargement. The lower extremity venous ultrasound was normal. Echocardiography indicated good left ventricular function, with no signs of right atrial overload or inferior vena cava dilation.
Table 1.
Laboratory data of the patient
| Reference range | Value | |||||
|---|---|---|---|---|---|---|
| day1 | day17 | day25 | day84 | day350 | ||
| < Urinalysis > | ||||||
| Protein | (–) | (4 +) | (4 +) | (4 +) | (4 +) | (1 +) |
| Occult blood | (–) | (2 +) | (2 +) | (2 +) | (1 +) | (2 +) |
| RBC (/HPF) | (–) | 10–19 | 5–9 | 5–9 | 10–19 | 5–9 |
| Protein (g/gCr) | (–) | 15.506 | 11.329 | 9.558 | 6.349 | 0.693 |
| Selectivity index | 0.09 | |||||
| < Complete blood count > | ||||||
| WBC (/μL) | 3300–8600 | 8740 | 17,670 | 17,390 | 11,340 | 11,360 |
| RBC (× 104/μL) | 386–492 | 386 | 388 | 325 | 288 | 406 |
| Hemoglobin (g/dL) | 11.6–14.8 | 12.3 | 12 | 10 | 9.1 | 12.7 |
| Hematocrit (%) | 35.1–44.4 | 36.6 | 35.7 | 30.1 | 26.6 | 38.5 |
| Platelet (× 104/μL) | 15.8–34.8 | 28.8 | 21.7 | 21 | 29.6 | 29.7 |
| < Coagulation > | ||||||
| APTT (s) | 11–14 | 30 | ||||
| PT (%) | 80–120 | 106.2 | ||||
| D-dimer (μg/mL) | 0–1 | 0.9 | ||||
| < Blood chemistry > | ||||||
| Total protein (g/dL) | 6.6–8.1 | 6.7 | 4.8 | 6.4 | ||
| Albumin (g/dL) | 4.1–5.1 | 3.2 | 1.9 | 2.0 | 2.1 | 3.0 |
| Creatinine (mg/dL) | 0.46–0.79 | 0.54 | 2.29 | 1.72 | 0.83 | 0.69 |
| Urea nitrogen, serum (mg/dL) | 8–20 | 25.9 | 154.2 | 67.3 | 25.7 | 22 |
| eGFR (mL/min/1.73m2) | 60–150 | 81.8 | 16.8 | 23 | 51.1 | 62.3 |
| Sodium (mEq/L) | 138–145 | 148 | 138 | 141 | 140 | 146 |
| Potassium (mEq/L) | 3.6–4.8 | 4.3 | 3.8 | 3.3 | 4.3 | 3.5 |
| Chlorinel (mEq/L) | 101–108 | 112 | 106 | 108 | 106 | 106 |
| Calcium (mg/dL) | 8.8–10.1 | 9.1 | 7.5 | 8.2 | 8.9 | |
| Phosphorus (inorganic) (mg/dL) | 2.7–4.6 | 3.5 | 3.2 | 3.7 | 2.3 | |
| CRP (mg/dL) | 0–0.14 | 0.11 | 0.02 | 0.05 | 0.06 | 0.42 |
| T-cho (mg/dL) | 142–248 | 319 | 433 | |||
| LDL-C (mg/dL) | 65–163 | 205.8 | 295.2 | 98.6 | ||
| HDL-C (mg/dL) | 48–103 | 70.9 | 82.5 | 79.1 | ||
| Hemoglobin A 1c (%) | 4.9–6.0 | 5.7 | ||||
| IgG (mg/dL) | 861–1747 | 1279 | ||||
| IgA (mg/dL) | 93–393 | 308 | ||||
| IgM (mg/dL) | 50–269 | 150 | ||||
| IgE (IU/mL) | 0–173 | 27.9 | ||||
| C3 (mg/dL) | 86–160 | 146 | ||||
| C4 (mg/dL) | 17–45 | 20 | ||||
| CH50 (U/mL) | 25–48 | 33.8 | ||||
| Antinuclear antibody | 0–39 | < 40 | ||||
| RF (IU/mL) | 0–15 | < 1.3 | ||||
| PR3-ANCA | (–) | (–) | ||||
| MPO-ANCA | (–) | (–) | ||||
| Anti-GBM antibody | (–) | (–) | ||||
| < Infection > | ||||||
| RPR | (–) | (–) | ||||
| TPHA | (–) | (–) | ||||
| Hbs-Ag | (–) | (–) | ||||
| HCV-Ab | (–) | (–) | ||||
Day1: at the initial visit, day17: at the initiation of hemodialysis, day25: before the initiation of Cyclosporine A, day84: at the discharge
RBC red blood cell, WBC white blood cell, APTT activated partial thromboplastin time, PT prothrombin time, CRP C-reactive protein, T-chol total cholesterol, LDL-C low-density lipoprotein cholesterol, HDL-C high-density lipoprotein cholesterol, IgG immunoglobulin G, IgA immunoglobulin A, IgM immunoglobulin M, IgE immunoglobulin E, C3 complement 3, C4 complement 4, CH50 50% haemolytic complement, RF rheumatoid factor, PR3-ANCA proteinase 3-ANCA, MPO-ANCA myeloperoxidase-ANCA, Annti-GBM antibody anti-glomerular basement membrane antibody, RPR rapid plasma reagin, TPHA Treponema pallidum hemagglutination, Hbs-Ag hepatitis B surface antigen, Hbs-Ab hepatitis B surface antibody, Hbc-Ab hepatitis B core antibody, HCV-Ab hepatitis C antibody
After her hospitalization, intravenous methylprednisolone pulses (500 mg/day, 3 days) were administered on day 3, followed by 40 mg of oral prednisolone (0.8 mg/kg/day). After the initiation of treatment, the urine protein level improved to 5.82 g/gCr on day 7. We performed a renal biopsy on day 8 (Fig. 1). Light microscopy of the biopsied sample showed 10 glomeruli, including 1 global sclerosis, and those did not include segmental sclerosis. Those showed normal-appearing glomeruli. A little interstitial edema and inflammation were noted and tubular necrosis was not observed. Immunofluorescence analysis revealed segmental mesangial deposits of immunoglobulin A (IgA). Electron microscopy revealed fusion of podocyte foot processes without any electron-dense deposits. Based on these pathological findings, a diagnosis of MCD associated with faint mesangial IgA deposits was made.
Fig. 1.
Pathological findings from the renal biopsy specimen. a Light microscopy showing normal-appearing glomeruli (hematoxylin–eosin stain, magnification × 300) b Immunofluorescence analysis showing segmental mesangial deposits of immunoglobulin A c Electron microscopy showing fusion of podocyte foot processes without electron-dense deposits
A progress chart is shown in Fig. 2. Her urine protein increased to 21 g/gCr on day 11. Her serum creatinine was 2.42 mg/dL. Her LDL-cholesterol level was 295.2 mg/dL, and atorvastatin 10 mg/day was initiated on day 15. The response to diuretics was poor, urine volume (UV) was about 400 mL/day, and her body weight increased. Although she received corticosteroids, hypoalbuminemia of 1.9 g/dL and proteinuria of 11.3 g/gCr were observed on day 16. We initiated hemodialysis on day 17. The second intravenous steroid pulse therapy was added from day 17–19. Due to hypoalbuminemia, we added 25% albumin infusion for four days (on day 18, 19, 21, 25). However, the urine protein increased to 13.0 g/gCr on day 22. We also started LDL-A on day 18 as an additional treatment modality. It was performed using hollow polysulfone fibers (Sulflux FP-05®; Kaneka Co. Ltd., Osaka, Japan) as the plasma separator and a dextran sulfate cellulose column (Liposorber LA-15; Kaneka Co. Ltd., Osaka, Japan) as the LDL absorber. Approximately 2900 mL of plasma was treated (nearly equal to body weight (kg)/13 × (1—hematocrit)). A total of seven LDL-A sessions were performed. After completing LDL-A, LDL-cholesterol level was 74.0 mg/dL. Her renal function improved and hemodialysis was discontinued on day 29. Her weight was 59.0 kg on day 16 (when hemodialysis was initiated) and 59.1 kg on day 29 (when hemodialysis was discontinued). Following seven sessions of LDL-A, her urine output increased rapidly, her weight decreased, and the lower limb edema showed marked improvement. Cyclosporine A (CyA) was initiated on day 29. Her creatinine level was 0.83 mg/dL and her urine protein was 6.349 g/gCr on day 84, then she was discharged on day 89. After discharge, proteinuria persisted at around 3.0–5.0 g/gCr and serum albumin around 2.0–2.5 g/dL for a few months. The proteinuria declined to 0.693 g/day on day 350, achieving incomplete remission type I, and outpatient follow-up continues with gradually tapering oral prednisolone.
Fig. 2.
Clinical course: change in the UP, serum creatinine level, and urine volume. After initiating LDL-A, the levels of UP and serum creatinine gradually decreased. She discontinued hemodialysis and achieved incomplete remission type I 350 days after admission. mPSL methylprednisolone, PSL prednisolone, CyA cyclosporine A, HD hemodialysis; LDL-A low-density lipoprotein apheresis, UP urine protein, Cr creatinine
Discussion
We herein report a 75-year-pld woman with steroid-resistant MCD who developed rapidly progressive renal dysfunction, ultimately requiring hemodialysis, where LDL-A led to a dramatic recovery of renal function. The patient experienced a rapid deterioration in kidney function, necessitating hemodialysis on day 17. Due to a lack of responsiveness to steroid treatment and persistent severe proteinuria, LDL-A was started on day 18. The administration of LDL-A resulted in a swift increase in urine output and a recovery of renal function, allowing for the discontinuation of hemodialysis. Improved renal function allowed for the safe initiation of CyA, and approximately one year later, proteinuria improved to incomplete remission type I.
This case report highlights the successful treatment of early LDL-A for steroid-resistant MCD with AKI needed hemodialysis in the elderly. MCD with AKI sometimes needs renal replacement therapy such as hemodialysis. AKI is induced by the damage of the water and solutes filtration function due to foot process fusion [2]. The fusion of foot processes in MCD reduces the total length of glomerular epithelial slit pores, leading to decreased permeability of glomerular capillaries to water and small solutes [7]. Additionally, in most severe AKI with protracted oliguria, a process of renal ischemia is considered, especially in aged and/or hypertensive patients with nephrosclerosis, an umbrella term that covers microvascular lesions that reduce the afferent arteriolar blood supply to the glomerular tuft [8, 9]. In some studies, it is shown that endothelin 1 (ET-1) levels elevated in renal tissue and in the urine of MCD [10]. ET-1 is the major renal peptide that exerts its biological activity by binding to ET(A) and ET(B) receptors. Those receptors are expressed by renal microvascular endothelial cells. When ET-1 activates those receptors, vasoconstriction is caused and then it can influence renal hemodynamics [11]. AKI is associated with enhanced kidney ET-1 expression in MCD [12]. A study reported LDL-A decreases the plasma ET-1 level [13]. It means LDL-A may improve AKI by reducing ET-1.
In Japan, a prospective cohort study (Prospective Observational Survey on Long-Term Effects of LDL-A on Drug-Resistant NS Syndrome; POLARIS) was conducted and LDL-A showed reasonable efficacy in treating NS refractory to initial drug therapy [14, 15]. A post hoc analysis of the POLARIS study investigated the efficacy of LDL-A for patients with impaired renal function. In the study, many patients who had moderately impaired ((≥ 30 to < 60 mL/min/1.73 m2) or severely impaired (< 30 mL/min/1.73 m2) renal function had recovered from NS and most of them had avoided end-stage renal failure at 2 years after treatment [16]. LDL-A may provide effective treatment and positive outcomes for patients with impaired renal function.
MCD commonly manifests with hyperlipidemia, characterized by significantly elevated LDL-cholesterol, very low-density lipoprotein cholesterol, LP(a), and triglycerides, with modest increase in high-density lipoprotein cholesterol. NS-induced hyperlipidemia and altered lipid metabolism contribute to cardiovascular and kidney disease progression [17]. LDL-cholesterol binding to the glomerular basement membrane increases permeability, leading to lipoprotein accumulation in mesangial cells, stimulating their proliferation and matrix production [18]. Filtered lipoproteins can undergo modifications in the nephron, potentially worsening tubulointerstitial disease [19]. Inflammatory stress exacerbates renal lipid accumulation, involving reactive oxygen species and ER stress. Increased intracellular lipids under inflammatory stress cause oxidative and ER stress, potentially contributing to renal injury and CKD progression [18]. Proteinuria also stimulates proinflammatory cytokine secretion by proximal tubular cells, leading to hypercytokinemia [19].
The mechanisms of LDL-A for NS were not only an improvement in hyperlipidemia but also a reduction of excessive activation of macrophages and inhibition of inflammatory cytokines. In NS, LDL-A immediately reduced elevated levels of IL-6, TNF-α, sCD40L, and IL-31 significantly, while the anti-inflammatory cytokine IL-10 increased [6]. LDL-A is considered to improve hypercytokinemia. In addition, the absorption of fluids that cause NS and recovery of sensitivity by inhibiting drug resistance are also thought to contribute to the improvement [19]. Moreover, serious adverse events of LDL-A are rare, occurring in only about 0.3% of treatments [20]. LDL-A is a relatively safe option.
LDL-A has also been applied for steroid-resistant NS due to FSGS [21]. Several studies showed that LDL-A may be effective for non-FSGS or for diabetic nephropathy [22]. POLARIS study showed LDL-A led reasonable efficacy in NS refractory to initial drug therapy. In this study, the rate of favorable outcomes of the immediate proteinuria-reducing in non-FSGS subjects treated with LDL-A was 50.0%, which is comparable to the rate in FSGS subjects [14, 15]. Nakatani et al. reported a steroid-resistant MCD case successfully treated with LDL-A on day 55 after the admission and reviewed 15 similar cases (9 reports), where 11/15 achieved NS remission and 4/11 complete remission, suggesting the efficacy of LDL-A [23]. Nishizono, et al. also reported a rapid complete remission in an MCD with Type I diabetes case treated with LDL-A on day 42 [24]. Terada, et al. reported a case series in which LDL-A was applied to patients with AKI due to MCD on day 21 or 24 after the initiation of steroid therapy respectively, resulting in rapid recovery of diuresis, withdrawal from hemodialysis, and remission of NS [25]. Furthermore, a relapsed MCD case after rituximab achieved complete remission with LDL-A and low-dose prednisolone [26]. In our case, LDL-A started on day 18 after the admission, leading to rapid improvement of renal dysfunction and gradual improvement in proteinuria, hyperlipidemia, hypoproteinemia. Though there are a lot of favorable results of LDL-A for MCD, the timing for initiating LDL-A is not well established. There are also no reports of LDL-A being initiated as early as in our case.
Although we believe that early LDL-A contributed to the improvement of AKI and NS, we cannot rule out the possibility that FSGS was differently diagnosed by renal biopsy in the first place. In some cases, those who have steroid-resistant MCD with persistent massive proteinuria, a repeat kidney biopsy sometimes shows lesions of FSGS [3, 27]. Furthermore, the persistent proteinuria of 3.0–5.0 g/day after LDL-A termination, followed by gradual improvement after about 1 year, suggests that CyA may have been effective in the long term.
In conclusion, we achieved rapid improvement of renal dysfunction and incomplete remission type I of MCD after the initiation of LDL-A. Especially in this case, LDL-A was started so early and it seems to be effective for an elderly patient with AKI and steroid-resistant MCD, and she could discontinue hemodialysis and reduce severe proteinuria. We suggest that early LDL-A initiation for elderly patients with AKI due to steroid-resistant MCD is a good alternative therapy.
Data availability
The datasets generated and/or analyzed during the current study are available from the corresponding author on reasonable request.
Declarations
Conflict of interest
The authors have declared that no conflict of interest exists.
Research involving human participants
This article does not contain any studies with human participants or animals performed by any of the authors.
Informed consent for publication
Informed consent was obtained from the individual participant.
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Associated Data
This section collects any data citations, data availability statements, or supplementary materials included in this article.
Data Availability Statement
The datasets generated and/or analyzed during the current study are available from the corresponding author on reasonable request.