Medical Reports & Case Studies

Acute Kidney Injury in Minimal Change Disease in Young Female: A Case Report

Parneet Kaur^1*, Lilit Gasparyan² and Akhil Jain^{3 *}Correspondence: Parneet Kaur, Department of Medical Science, Sri Guru Ram Das Institute of Medical Sciences and Research,Amritsar, India, Email:

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Introduction

Nephrotic syndrome is the derangement in renal glomerular function which exhibits as an aggregate of edema, massive proteinuria, and hypoalbuminemia. Despite minimal change disease (MCD) is the most common cause of nephrotic syndrome in children, it is accountable for only 10-15 % of cases of nephrotic syndrome in adults [1]. Nephrotic syndrome is associated with various complications, especially in adults. One-quarter of patients may have acute kidney injury (AKI). These patients are mostly hypertensive elderly males[2]. We hereby report a case of a 30-year-old normotensive woman who developed AKI in the setting of MCD.

Acute kidney injury

A 30-year-old Indian female came to the outpatient clinic with generalized swelling all over the body for 1 week. The swelling began in the periorbital area and progressed gradually leading to generalized anasarca. Her past medical history was significant for intermittent usage of NSAIDs for the last 5 years for body aches and muscle soreness. Vitals were within normal limits and physical examination was remarkable only for periorbital and pedal edema (3+). Laboratory parameters revealed serum creatinine of 2.80 mg/dl, BUN of 79.2 mg/dl, serum albumin of 2.04 gm%, total protein of 4.47 gm%, total cholesterol of 198.6 mg/dl, and serum triglycerides of 425 mg/dL. Twenty-four-hour urine protein assay was 6.93 grams. Serologic studies for HIV, hepatitis B, and hepatitis C were negative. Chest x-ray showed bilateral pleural effusion, and abdominal ultrasound showed an edematous gallbladder with moderate ascites. The patient’s fluid overload initially was treated with diuretics along with intravenous albumin. The patient’s edema regressed initially in the first week but recurred rapidly. Therefore, a renal biopsy was performed. The light microscopic histopathology revealed luminal dilatation of tubules, epithelial simplification with a few tubules showing luminal granular material with normal glomeruli without any basement membrane thickening, segmental sclerosis, any proliferative lesion or interstitial changes. Immunofluorescence showed seven glomeruli that were negative for IgG, IgA, IgM, Kappa, Lambda, C3, and C1q. No extraglomerular staining was seen. Thus, the diagnosis of acute tubular injury with minimal change disease was made. The patient was treated with prednisolone 1mg/kg body weight. Her edema regressed in 2 weeks. Her serum creatinine dropped to 1.10 mg/dL. Moreover, her BUN, serum albumin, and protein levels also showed satisfactory improvement. No further relapses were observed in followup outpatient visits of the patient for up to 4 months of observation.

Discussion

Minimal change disease is characterized by diffuse effacement and flattening of the foot processes of the podocytes which we can see on electron microscopy. This flattening causes massive proteinuria, selectively albuminuria, which leads to hypoalbuminemia and anasarca. Acute kidney injury in the background settings of MCD has been mostly reported in male, elderly, and hypertensive patients, and these were also reported to have lower serum albumin and more proteinuria as compared to the patients, who do not have AKI [2,3]. AKI was reported in 34% of the patients out of 277 with idiopathic nephrotic syndrome[2]. Waldman et al. reported Acute Renal Failure (ARF) as a complication in 25 % of the MCD patients in a retrospective study of 95 adults [3]. In contrast to presentations in these reports, our case report stands out unique in terms of the patient being young and female and without any pre-existing hypertension. There is no similar case that has not been reported in the literature before.

The causative factors, responsible for AKI in nephrotic syndrome, include Acute Tubular Necrosis (ATN), acute interstitial nephritis due to NSAIDs, ciprofloxacin, renal vein thrombosis, or infectious diseases like HIV [4]. Smith et al. reported ATN in 65% of patients on histopathological examination among 75 ARF patients with MCD [5]. The pathophysiologic mechanism responsible for kidney injury with MCD in our case can be explained by significantly decreased oncotic pressure, as a result of albuminuria and hypoalbuminemia, leading to a decrease in intravascular volume and third space loss in the form of bilateral pleural effusion. Glomerular capillary-basement membrane barrier disruption, leading to massive proteinuria in the form of albuminuria, majorly causes protein overload of tubular epithelial cells. Abbate and colleagues have reviewed the various mechanisms by which proteinuria can cause progressive renal damage. Activation of inflammatory pathways by ultra-filtered protein load has been proposed for progressive tubular damage in proteinuric patients [6]. Renal biopsy is the first step in the evaluation of adults having idiopathic nephrotic syndrome in contrast to the children where biopsy is only performed if features or clinical non-responsiveness to steroids suggest an alternate diagnosis [1]. The management of AKI in patients presenting with edema in MCD begins with diuretics. The role of albumin is controversial, and it is only used if the patient is not responsive to the use of two diuretics [4]. Along with supportive therapy for AKI, management of the first episode of MCD with prednisone at a dose of 1 mg/kg is recommended. Most of the patients respond by 4 weeks, however, it is recommended to give treatment for at least 16 weeks before declaring a patient steroid resistant. A repeat renal biopsy may be advisable to look for an alternate diagnosis, but once steroid resistance is established in MCD alternative therapies with Cyclophosphamide, Cyclosporine, Tacrolimus can be tried [7]. Considering the non-availability of an electron microscope at the local or regional level and the high cost involved for overboard transportation of biopsy specimens, we proceeded with treatment based on normal glomerulus found on light microscopic exam, no staining on immunofluorescence, and a high index of clinical suspicion of MCD. The patient responded well to the treatment and her creatinine level and serum albumin improved. There were no relapses seen after this episode.

Conclusion

Minimal change disease with heavy proteinuria can be a cause of renal tubular disruption leading to AKI. Though more common in hypertensive, elderly male persons, such a combination may be present at a younger age as well depending on the degree of proteinuria. A high index of suspicion coupled with renal biopsy establishes the diagnosis, and prompt administration of steroids can resolve the basic pathophysiology of MCD, thereby eradicating proteinuria and proteinuria related kidney injury.

References

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