#2907 ASYMPTOMATIC NEPHROTIC SYNDROME: AN INTERESTING PRESENTATION OF ADULT ONSET MINIMAL CHANGE DISEASE

Abstract

Abstract Background and Aims Minimal change disease (MCD), a predominantly pediatric disease, is less common in adults. Patients often present with florid hypervolemia, manifested by significant lower extremity edema, anasarca, pericardial effusion or pleural effusion. Herein, we present a case of newly diagnosed MCD in an elderly gentleman with an atypical presentation. Method A 69 year old male with hypertension and benign prostate hypertrophy presented to the emergency department (ED). He was noted to have abnormal labs at an outside clinic on routine testing and was directed to the ED. In the ED, he was found to have a serum creatinine (SCr) of 10.89 mg/dL. Initial urine studies also revealed proteinuria of 11g/g with 6.5 g/g of albuminuria. Other initial labs were significant for a potassium of 4.5 mEq/L, BUN 126 mg/dL and albumin 2.2 g/dL with normal liver enzymes. Renal ultrasound was unremarkable. Upon further discussion with the patient, he endorsed long term daily use of diclofenac for many months. He stated that he stopped diclofenac three weeks prior to presentation. He denied any proton pump inhibitor or recent antibiotic use. He denied any fevers, nights sweats or weight loss to suggest Type B symptoms. There was no personal kidney disease history nor family history of kidney disease. He was a non-alcoholic and non-smoker. We continued to hold further non-steroidal anti-inflammatory medications as well as other nephrotoxic medications. Although patient had elevated SCr and azotemia, he did not meet any acute indications for dialysis and we continued to manage the patient conservatively. Serologies were negative for ANA, ANCA, Anti-GBM, HIV, hepatitis B and C, as well as antiPLA2R. Serum protein electrophoresis, kappa to lambda ratio, complements 3 and 4 were all within normal values. A kidney biopsy was revealing for patchy interstitial inflammatory infiltrate containing mononuclear cells admixed with few eosinophils on light microscopy as well as diffuse foot process effacement on electron microscopy (Figure 2). The patient had a one-week hospital stay with improvement of SCr to 2.29 mg/dL without any prednisone or treatment for MCD. Spot urine protein improved to 7.4 g/g by time of discharge. At clinic follow up 2 weeks later his creatinine had improved to 1.1 mg/dL with UPCR of 0.4 g/g. Results MCD is a podocytopathy that can occur in up to 10% of adults with nephrotic syndrome [1]. Secondary MCD has been reported with NSAIDs. Steroids are the first line therapy for MCD and can lead to remission in the majority of the cases. In patients who do not respond to steroids, calcineurin inhibitors or mycophenolate can be used. Conclusion Our patient presented with biopsy proven-MCD that was presumed to be secondary to diclofenac. His clinical presentation was not characteristic of nephrotic syndrome with no edema. Few reports exist of spontaneous remission in these patients with most of the patient requiring steroids. While it is uncommon for patients with MCD to spontaneously resolve, not all patients with NSAID-induced MCD require treatment and these patients could be monitored conservatively.