Pseudo-renal failure with hyponatremia and proteinuria after gynecologic surgery: a case report with literature comparison

Abstract

Background

Acute kidney injury (AKI) is defined by an increase in serum creatinine according to the Kidney Disease: Improving Global Outcomes criteria. In contrast, pseudo-renal failure is a rare condition characterized by azotemia and electrolyte imbalance that mimic AKI, while the actual renal function remains preserved. Because of its rarity and nonspecific presentation, pseudo-renal failure is often misdiagnosed as true AKI. We report a rare case of pseudo-renal failure caused by intraperitoneal bladder rupture following gynecologic surgery. This case is unique in that pseudo-renal failure was accompanied by severe hyponatremia and nephrotic-range proteinuria despite the absence of significant glomerular pathology, highlighting an important diagnostic pitfall.

Case presentation

A 49-year-old woman presented with progressive renal dysfunction and persistent mild lower abdominal discomfort two weeks after total laparoscopic hysterectomy with bilateral salpingo-oophorectomy for uterine leiomyoma. Laboratory tests revealed markedly elevated blood urea nitrogen (68.2 mg/dL) and creatinine (4.48 mg/dL), with relatively preserved cystatin C (1.34 mg/L), severe hyponatremia (123 mmol/L), and nephrotic-range proteinuria (7.9 g/day). A kidney biopsy was performed to evaluate for an underlying glomerular disease; however, it revealed only minor glomerular changes with no significant pathological abnormalities. Abdominal ultrasonography revealed moderate ascites without other remarkable findings. To investigate the cause of the ascites, diagnostic paracentesis was performed, which revealed an ascitic creatinine level higher than the serum creatinine level, suggesting urinary ascites. Consequently, computed tomography (CT) cystography confirmed urinary leakage caused by intraperitoneal bladder rupture. The patient underwent the surgical repair following Foley catheter placement. Her renal function normalized postoperatively, with resolution of hyponatremia and a reduction in proteinuria.

Conclusions

This case highlights the importance of recognizing pseudo-renal failure as a differential diagnosis of unexplained azotemia, particularly in patients with recent pelvic surgery. The coexistence of elevated serum creatinine with relatively preserved cystatin C, ascites, hyponatremia, and nephrotic-range proteinuria should raise suspicion for urinary tract injury. Measurement of ascitic fluid creatinine and CT cystography are key diagnostic tools for genitourinary trauma that can prevent unnecessary invasive procedures and guide timely therapeutic interventions. Ultimately, awareness of this entity enables prompt diagnosis and favorable clinical outcomes for patients.

Background

Acute kidney injury (AKI) is defined by rise in serum creatinine according to the Kidney Disease Improving Global Outcome (KDIGO) guidelines. In a different context, there is also the concept of pseudo-renal failure, which mimics acute kidney injury. In pseudo-renal failure, azotemia, metabolic acidosis, and hyperkalemia may be present, but the actual renal function remains normal [1]. It may occur due to substances that affect creatinine secretion or measurement, as well as urinary leakage into the peritoneal cavity caused by urinary tract injury [1–3].

Pseudo-renal failure is a rare condition, so it can be easily missed during clinical assessment and mistaken for acute kidney injury due to similar laboratory findings. Therefore, we conducted an analysis and review of a case of pseudo-renal failure caused by bladder rupture following gynecologic surgery to highlight the significance of this concept. This case is unique in that pseudo-renal failure was accompanied by severe hyponatremia and nephrotic-range proteinuria despite the absence of significant glomerular pathology, highlighting an important diagnostic pitfall.

Case presentation

A 49-year-old Korean woman was admitted to the hospital via the emergency department due to worsening renal function. She had experienced persistent mild lower abdominal discomfort for one week. Her medical history included uterine leiomyoma, for which she had undergone total laparoscopic hysterectomy (TLH) with bilateral salpingo-oophorectomy (BSO) at a local gynecology clinic two weeks prior to admission. She had no other known underlying medical conditions, no history of smoking, alcohol, or drug abuse, and no family history of kidney disease.

Her initial vital signs were as follows: blood pressure 126/83 mmHg, heart rate 92 beats/min, respiratory rate 18 breaths/min, and body temperature 36.2 ℃. No remarkable findings were noted on physical examination. Initial laboratory findings revealed a blood urea nitrogen (BUN) level of 68.2 mg/dL, creatinine 4.48 mg/dL, cystatin C 1.34 mg/L, sodium 123 mmol/L, potassium 5.2 mmol/L, albumin 4.5 g/dL, aspartate aminotransferase (AST) 18 IU/L, alanine aminotransferase (ALT) 9 IU/L, and total bilirubin 0.48 mg/dL. Urinalysis revealed microscopic hematuria (color yellow, 10–29 red blood cells (RBCs) /HPF), urine protein-to-creatinine ratio 977 mg/g creatinine, urine creatinine 57.34 mg/dL, and urine sodium 53 mmol/L (Table 1).

Table 1.

Serum and urine laboratory findings

Parameter	Result	Reference range
Blood
Hemoglobin (g/dL)	13	12–16
White blood cell count (×103/µL)	7.5	4.5–11.0
Neutrophils (%)	69.2	40–75
Lymphocytes (%)	21.2	13–44
Monocytes (%)	7.8	2.4–11.8
Platelets (×103/µL)	283	150–440
BUN (mg/dL)	68.2	7–20
Creatinine (mg/dL)	4.48	0.5–1.1
Cystatin C (mg/L)	1.34	0.51–1.05
Osmolality (mOsmol/kg)	278	289–305
Sodium (mmol/L)	123	135–145
Potassium (mmol/L)	5.2	3.5–5.5
Chloride (mmol/L)	95	98–110
Total CO2 (mmol/L)	22	21.0–31.0
Total protein (g/dL)	8.4	6.0–8.0
Albumin (g/dL)	4.5	3.3–5.1
Calcium (mg/dL)	9.9	8.8–10.6
Phosphorus (mg/dL)	9.5	2.3–4.7
AST (IU/L)	18	10–36
ALT (IU/L)	9	5–36
Total bilirubin (mg/dL)	0.48	0.2–1.2
C-reactive protein (mg/L)	< 5.00	0–5
Urine
Urine specific gravity	1.019	1.005–1.030
Blood on urine dipstick test	1+	-
Protein on urine dipstick test	2+	-
Microscopic RBC (/HPF)	10–29	0–4
Protein/creatinine ratio (mg/gCr)	977	< 150
Osmolality (mOsmol/kg)	290	300–900
Creatinine (mg/dL)	57.34	20–320
Sodium (mmol/L)	53	40–220
Potassium (mmol/L)	26.9	25–120
Chloride (mmol/L)	40	110–250

Abbreviations: BUN Blood urea nitrogen, CO_2, Carbon dioxide, AST Aspartate aminotransferase, ALT Alanine aminotransferase, RBC Red blood cell

Prerenal AKI was initially suspected based on reduced oral intake after surgery, elevated serum BUN and creatinine levels, and hypoosmolar hyponatremia. Therefore, intravenous normal saline was continuously administered over several days; however, renal function did not improve, hyponatremia persisted, and the patient continued to complain of abdominal discomfort. As the patient presented with significantly impaired renal function, contrast-enhanced imaging was deferred, and instead, kidney-adrenal-bladder ultrasonography was performed. The sonographic findings revealed no evidence of hydronephrosis, and the bladder appeared unremarkable without signs of wall thickening or masses. Furthermore, no other structural abnormalities of the urinary tract were identified, and a moderate amount of ascites was noted on examination.

In addition, hyponatremia at presentation was suspected to contribute to the patient’s poor oral intake and abdominal discomfort. Although ascites was present, the patient appeared clinically euvolemic, and there was no history of medication use associated with hyponatremia. To evaluate the cause, serum and urine osmolality and urinary electrolytes were assessed. Serum osmolality was 278 mOsmol/kg, urine osmolality 290 mOsmol/kg, and urine sodium 53 mmol/L, suggesting impaired free water excretion. A 24-hour urine study revealed significant proteinuria (7,917 mg/day; microalbumin 6,444 mg/day). Serial spot urine testing demonstrated dynamic changes in proteinuria, with the urine protein-to-creatinine ratio increasing from 977 mg/g creatinine at admission to a peak value of 17,067 mg/g creatinine on hospital day 7. Based on these findings, a kidney biopsy was performed under the clinical impression of glomerulonephritis (GN) or acute tubular necrosis (ATN), but it revealed only minor glomerular changes with no global sclerosis (0 out of 9 glomeruli).

To relieve the patient’s abdominal discomfort associated with ascites, large-volume paracentesis (3,000 mL) was performed with albumin replacement (20% albumin 100 mL) administered after procedure. Ascitic fluid analysis obtained during paracentesis revealed an albumin concentration of 0.54 g/dL (542 mg/dL). The serum albumin level measured one day prior to paracentesis was 3.6 g/dL, resulting in a serum–ascites albumin gradient (SAAG) of 3.06. Other ascitic fluid tests, including cultures, adenosine deaminase (ADA), and lipopolysaccharide-binding protein (LBP), showed no remarkable findings. However, the creatinine level in the ascitic fluid sample was 11.08 mg/dL, which exceeded the serum creatinine level, suggesting the presence of urinary ascites.

Computed tomography (CT) cystography was then performed to evaluate suspected peritoneal urinary leakage, and the diagnosis of intraperitoneal bladder rupture was confirmed (Fig. 1a). Therefore, a Foley catheter was initially placed, followed by surgical repair of the bladder injury in collaboration with the urology department. The patient tolerated all interventions well. Before catheter placement, the patient maintained spontaneous voiding with a urine output of approximately 1.5–2.5 L/day, remaining non-oliguric. After catheter placement and surgical repair, urine output increased to over 3.0 L/day, accompanied by rapid normalization of serum creatinine and sodium levels. In addition, proteinuria improved markedly, with the urine protein-to-creatinine ratio decreasing to 362 mg/g creatinine by postoperative day 1. Follow-up CT cystography was also performed on postoperative day 9, and no intraperitoneal contrast leakage was observed (Fig. 1b). The patient remained clinically stable and was subsequently discharged without any complications. No adverse or unanticipated events occurred during hospitalization. The temporal relationships among clinical interventions, urine output, renal function, and changes in proteinuria during hospitalization are summarized in Table 2.

Fig. 1.

CT cystography before and after surgical repair of bladder injury. (a) Preoperative CT cystography demonstrates contrast extravasation from the bladder into the pelvic cavity, consistent with intraperitoneal bladder rupture. (b) Postoperative CT cystography shows resolution of contrast leakage following surgical repair of the bladder

Table 2.

Temporal changes in laboratory parameters and clinical course during hospitalization

Hospitalization Days (HD)	HD #1	HD #3	HD #4	HD #5	HD #7	HD #8	HD #9 (Op)	HD #10 (POD #1)	HD #12 (POD#3)	HD #14 (POD#5)
Laboratory tests
Serum creatinine (mg/dL)	4.48	3.3	3.25	3.52	3.85		0.62	0.63	0.55
Serum cystatin C (mg/L)	1.34	1.02	0.81	1.1	0.95			0.64	0.62
Serum sodium (mmol/L)	123	125	128	124	125	127	132	134	141	138
U/A protein	2+	3+	2+	3+	3+			1+
Random urine protein (mg/dL)	56.0	223.1			481.3			53.9
Random urine creatinine (mg/dL)	57.34	26.6			28.2			148.75
Random urine protein/creatinine ratio (mg/gCr)	977	8387			17,067			362
24 h urine protein (mg/day)				7917
24 h urine microalbumin (mg/day)				6443.8
24 h urine creatinine (mg/day)				707.9
Fluid balance parameters
Total intake (mL)	4335	3379	1734	3300	2319	2700	1750	3267	2500	3055
Urine output (voiding) (mL)	2500	1700	2250	2300	1880	1800
Urine output (foley) (mL)							1525	1600	2250	3350
Postoperative drainage (mL)							150	310	230	74
Paracentesis volume (mL)			3000			3000
Albumin infusion (100 mL of 20% solution)			Y			Y

HD #9 corresponds to the day of surgical repair for the intraperitoneal bladder rupture. Laboratory data obtained on the operation day reflect postoperative values. Urine output (voiding) represents spontaneous voided urine prior to Foley catheter placement; urine output (foley) represents drainage via indwelling Foley catheter after surgery. Y indicates that albumin infusion was administered

Abbreviations: HD hospital day, OP operation, POD postoperative day, U/A urinalysis

Discussion and conclusions

In this case, pseudo-renal failure, characterized by elevations in serum urea and creatinine without actual renal injury, was suggested. Pseudo-renal failure can occur through several mechanisms, including urinary leakage into the peritoneal cavity with reabsorption of creatinine following upper or lower urinary tract rupture—most commonly bladder rupture—or the use of medications such as cimetidine, trimethoprim, and salicylates that inhibit the tubular secretion of creatinine [1, 2]. Also, certain drugs or endogenous substances may interfere with the Jaffe method of creatinine measurement. While compounds such as acetone can cause positive interference resulting in falsely elevated creatinine levels [3], bilirubin is known to cause negative interference, leading to falsely decreased creatinine values when measured using the Jaffe method [4].

Bladder rupture can result from blunt force trauma, most frequently due to motor vehicle accidents, which account for the majority of cases, or from iatrogenic injuries associated with gynecological, obstetrical, colorectal surgeries, and urologic procedures [5]. Urinary tract injuries occur in approximately 0.3% to 0.8% of gynecologic surgeries, with bladder injuries accounting for 0.05% to 0.66% of cases. Bladder injury occurs most frequently in hysterectomy procedures among gynecologic surgeries [6]. Although spontaneous bladder rupture is rare, it can occur and is associated with a high mortality rate [7].

To provide context, we reviewed nine recent cases of bladder rupture with pseudo-renal failure (Table 3). Serum creatinine in these reports varied widely (1.76 to approximately 20 mg/dL), and BUN similarly showed marked elevation in many cases despite preserved renal function. Notably, when reported, hyponatremia was mild (e.g., 128–135 mmol/L in a few cases)[13]. Proteinuria was rarely detailed, and when present, far below the nephrotic range [1, 12].

Table 3.

Published cases of bladder rupture with pseudo-renal failure and key laboratory findings

Author	Year	Sex/Age	Cause of rupture	Peak renal function	Electrolyte	Urinalysis
Shamsudheen M et al. [1]	2022	M/28	Road traffic accident	BUN 322 mg/dL, Cr 12.95 mg/dL	K 6.0 mmol/L	Proteinuria (spot 1.8 g/gCr), microscopic hematuria
Cheung D et al. [8]	2021	M/40	Fall while walking	BUN 26 mg/dL, Cr 1.76 mg/dL	K 5.2 mmol/L	Gross hematuria, protein (–)
Zhou C et al. [9]	2015	F/34	Spontaneous (uterine compression)	BUN 90.62 mg/dL, Cr 5.86 mg/dL	Na 135 mmol/L	Protein (–)
Ruggeri M et al. [10]	2021	Young adult	Road accident	BUN 93 mg/dL, Cr 6.94 mg/dL	Na 141 mmol/L	N/A
Cervantes CE et al. [11]	2020	M/39	Post-laparoscopic hysterectomy	BUN 45 mg/dL, Cr 7.4 mg/dL	Na 134 mmol/L	Microscopic hematuria
Mark A et al. [12]	2017	M/24	Spontaneous rupture	Cr 11.44 mg/dL	N/A	Proteinuria 500 mg/dL
Shekar A et al. [13]	2020	M/63	Forniceal rupture (bladder cancer)	Cr 20 mg/dL	K 9.0 mmol/L, Na 128 mmol/L	N/A
Jiang R et al. [14]	2023	F/85	Spontaneous rupture (remote hysterectomy + RT/CTx)	Cr 4.16 mg/dL	Na 133 mmol/L	N/A
Newman M et al. [15]	2022	M/62	Fall on ice	Cr 7.4 mg/dL	N/A	N/A

Abbreviations: RT/CTx Radiotherapy/Chemotherapy

In contrast, our patient exhibited nephrotic-range proteinuria (7.9 g/day) and marked hyponatremia (123 mmol/L)—features not described to this extent in prior reports. This combination initially suggested a primary glomerular disease and even led to a kidney biopsy before the correct diagnosis was made.

When bladder rupture occurs, urine leaks into the peritoneal cavity, resulting in urinary ascites. Urinary ascites typically contains high concentrations of creatinine, urea, and potassium, but relatively low sodium [16, 17]. Therefore, small molecules such as creatinine, urea, and potassium can diffuse from the peritoneal cavity back into the bloodstream—a process known as reverse auto-peritoneal dialysis—in contrast to conventional peritoneal dialysis [16, 17]. This transperitoneal movement raises serum creatinine, urea, and potassium despite preserved renal function, thereby mimicking acute kidney injury and producing the clinical picture of pseudo-renal failure. In contrast, sodium diffuses in the opposite direction, moving from the plasma, where its concentration is higher, into the peritoneal cavity until equilibrium is achieved. The resulting decline in serum sodium can lead to hyponatremia, and the macula densa senses the low sodium concentration in both serum and tubular fluid, triggering activation of the renin–angiotensin–aldosterone system (RAAS). RAAS activation promotes distal tubular sodium reabsorption, further decreasing urinary sodium excretion and perpetuating the cycle of hyponatremia [8, 18, 19].

Although nephrotic-range proteinuria was observed in this case, isolated tubular dysfunction is unlikely to account for protein excretion of this magnitude in the absence of glomerular injury. Instead, the proteinuria should be interpreted with caution, as it likely represents an apparent and transient phenomenon rather than true nephrotic syndrome. The markedly elevated 24-hour urinary protein excretion may reflect the cumulative effect of continuous leakage of protein-rich material into the bladder over time. In the setting of bladder rupture, blood, inflammatory exudates, desquamated urothelial cells, and other proteinaceous debris originating from the rupture site may mix directly with urine, contributing to apparent proteinuria that does not originate from glomerular filtration. While a spot urine protein-to-creatinine ratio represents a single time-point measurement, a 24-hour urine collection integrates protein contributions throughout the entire collection period, potentially leading to overestimation of total urinary protein excretion. In addition, albumin replacement administered during hospitalization may have influenced urinary protein measurements to some extent; however, the temporal pattern of proteinuria—particularly the decline observed after subsequent albumin administration and definitive surgical repair—does not support albumin infusion as the primary driver of the observed nephrotic-range proteinuria. The absence of glomerular lesions on kidney biopsy and the rapid resolution of proteinuria following bladder decompression and surgical repair further support a non-glomerular origin for the observed proteinuria.

An important clinical nuance is that our patient remained able to void spontaneously and reported only mild lower abdominal discomfort despite the presence of moderate ascites. This relatively subtle presentation differs from the classical picture of bladder rupture—often characterized by severe abdominal pain, inability to void, or overt peritoneal signs—and underscores the need to consider urinary tract injury even when classical symptoms are absent [20].

During the initial evaluation of a patient, diagnostic paracentesis with measurement of ascitic creatinine (ascites-to-serum ratio > 1.0) can serve as a key non-invasive clue to bladder rupture [21]. Similarly, a relatively stable serum cystatin C in the face of elevated creatinine (high serum creatinine-to-cystatin C ratio) can further support the diagnosis of pseudo-renal failure [14].

CT cystography can be the gold standard for diagnosing bladder rupture owing to its sensitivity and ability to detect other coexisting intra-abdominal pathologies [22]. For the treatment of bladder rupture, surgical repair is recommended for all intraperitoneal bladder ruptures and for some complicated extraperitoneal bladder injuries [5, 23]. Follow-up cystography is recommended to verify adequate healing of the bladder after surgery [24]. On the other hand, non-operative management consisting solely of bladder drainage with catheter placement may be an appropriate and sufficient treatment approach for uncomplicated extraperitoneal or spontaneous bladder ruptures [5, 24]. Standard therapy consists of maintaining bladder catheterization for approximately two to three weeks; however, extended drainage may be warranted depending on the clinical context [23, 24].

This case underscores that nephrotic-range proteinuria and significant hyponatremia can accompany urinary ascites—features that closely mimic primary glomerular disease but, in this setting, point toward pseudo-renal failure secondary to bladder rupture. First, obtaining a thorough medical and surgical history, including recent pelvic or abdominal procedures, can be helpful in evaluating for urinary tract injury. Clinicians should also consider pseudo-renal failure in the differential diagnosis when serum creatinine is unexpectedly elevated with normal or relatively preserved cystatin C, ascites, hyponatremia, and nephrotic-range proteinuria following abdominal or pelvic surgery. In such contexts, paracentesis with ascitic creatinine measurement and serum cystatin C assessment can provide supportive information, potentially reducing unnecessary invasive testing and guiding timely management for favorable patient outcomes. As this is a single-case report, further accumulation and evaluation of similar cases are needed to broaden the clinical spectrum of this condition. Ultimately, increased clinical awareness through continued reporting may play a crucial role in improving diagnostic accuracy and guiding appropriate patient management in cases of urinary tract injury.

Abbreviations

ADA

Adenosine deaminase

AKI

Acute kidney injury

ALT

Alanine aminotransferase

ATN

Acute tubular necrosis

AST

Aspartate aminotransferase

BSO

Bilateral salpingo-oophorectomy

BUN

Blood urea nitrogen

CO₂

Carbon dioxide

CT

Computed tomography

CTx

Chemotherapy

GN

Glomerulonephritis

KDIGO

Kidney Disease Improving Global Outcomes

LBP

Lipopolysaccharide-binding protein

RAAS

Renin–angiotensin–aldosterone system

RBC

Red blood cell

RT

Radiotherapy

SAAG

Serum-ascites albumin gradient

TLH

Total laparoscopic hysterectomy

Author contributions

SJY was the major contributor in writing the manuscript. JEK critically revised and approved the final manuscript. All authors read and reviewed the final manuscript.

Funding

None.

Data availability

No datasets were generated or analysed during the current study.

Declarations

Ethics approval and consent to participate

This case report was conducted in accordance with the ethical standards of the institutional and national research committees and with the principles of the Declaration of Helsinki. This study was approved by the Institutional Review Board of Korea University Guro Hospital (IRB No. 2025GR0253).

Consent for publication

The patient gave permission for publication of this case and data with the written informed consent form.

Competing interests

The authors declare no competing interests.