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Revisiting Acute Kidney Injury in Minimal Change Disease a Case Report and Review of Literature

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Revisiting Acute Kidney Injury in Minimal Change Disease a Case Report and Review of Literature ARC Journal of Nephrology Volume 2, Issue 1, 2017, PP 1-5 www.arcjournals.org Revisiting Acute Kidney Injury in Minimal Change Disease a Case Report and Review of Literature Dr. Tena Abraham1, Dr. Shobhana Nayak –Rao2*, Dr. Pradeep Shenoy M3 1Postgraduate in General Medicine, Dept of General Medicine, K .S. Hegde Medical Academy, Medical Sciences Complex, Derlakatte, Mangalore, Karnataka, INDIA 2Associate Prof and Head, Dept of Nephrology, K.S. Hegde Medical Academy, Medical Sciences Complex, Derlakatte Mangalore, Karnataka, INDIA 3Assistant Prof, Dept of Nephrology. K.S. Hegde Medical Academy, Medical Sciences Complex, Derlakatte Mangalore, Karnataka, INDIA *Corresponding Author: Dr. Shobhana Nayak –Rao, Associate Prof and Head, Dept of Nephrology K.S.Hegde Medical Academy E-mail: [email protected] Abstract: The occurrence of renal failure has been believed to be a common complication of nephrotic syndrome associated with minimal change disease in children. In adults though, it has been relatively more infrequently documented than in children. Acute kidney injury (AKI) has been described in nephrotic syndrome in literature and has been associated with older age, systolic hypertension, vascular disease and increasing severity of nephrotic syndrome. The underlying pathophysiology responsible for the reduction of glomerular filtration rate (GFR) has been a matter of debate. We present a case of an elderly patient who presented with worsening renal failure and review the available literature on this entity of AKI in adult minimal change nephrotic syndrome. Keywords: Minimal change disease, nephrotic syndrome, adult, renal failure 1. INTRODUCTION patients and also look at the outcome of patients who develop AKI during the course of the The occurrence of renal failure has been illness. believed to be a common complication of nephrotic syndrome associated with minimal 1.1. Case change disease in children. In adults though, it A 75 year old male without any significant past has been relatively more infrequently medical history presented to us with one week documented than in children. Acute kidney history of progressive swelling of hands and injury (AKI) has been described in nephrotic feet and weight gain of > 10 kgs in the previous syndrome in literature since 1966 with more two weeks prior to admission. He had also noted than 85 cases reported so far(1,2). It has been slightly decreased urinary frequency and associated with older age, systolic hypertension, quantity of urine during this period. He did not vascular disease and increasing severity of report any preceeding h/o sore throat, arthralgia, nephrotic syndrome (3, 4). The underlying myalgia, skin rashes, hematuria, dysuria or h/o pathophysiology responsible for the reduction of any ingestion of any NSAID’s or any other glomerular filtration rate (GFR) has been alternative medication use. The patient did not proposed by Lowenstein et al (5) to be due to smoke or consume alcohol. Physical interstitial oedema of kidney also termed as examination revealed an elderly male weighing nephrosarca causing vascular or tubular 67 kgs (previous recorded weight 55 kgs ) , occlusion and a subsequent filtration failure. blood pressure of 150/90mm of Hg, pulse rate of However this has been debated in some reports 82/min, respiratory rate 18/min. There were 3+ and other mechanisms have been proposed (6). pitting edema till upper thighs and sacral edema. We present a case of an elderly patient who There were no skin rashes or lymphadenopathy presented with worsening renal failure and and all pulses were equally felt. Other than review the available literature on this entity of decreased breath sounds at both lung bases, the AKI in adult minimal change nephrotic remainder of the physical examination was syndrome including the known pathogenetic unremarkable. On admission, his blood urea mechanisms that lead to renal failure in these 67mg/dl, with a serum creatinine of 1.6mg/dl ARC Journal of Nephrology Page | 1 Revisiting Acute Kidney Injury in Minimal Change Disease- a Case Report and Review of Literature with normal serum electrolytes. Urine analysis 11 viable glomeruli and was negative for IgG, at presentation had 4+ proteins, 5-10 IgA, IgM, C3, C1q, kappa and lambda chains. WBC/HPF, no RBC and no casts. Hematology A diagnosis of minimal change disease with investigations revealed hemoglobin of 1.3gm/dl, mild acute tubular injury was made and total WBC count of 11,000/cmm, normal treatment was started with prednisolone 1mg/kg differential and platelet counts. An ultrasound daily basis. Over the next two weeks after abdomen did not reveal any organomegaly, admission and treatment initiation, the PCV normal kidney size (RK10.2X3.2cms, LK progressed to 9.09mg/dl with drop in estimated 11.0X3.cms) with normal cortical echogenicity GFR to 5.7ml/min. Volume overload persisted and no hydronephrosis. Total serum protein was despite albumin infusions, salt and water reduced at 4.5gm/dl with serum albumin restriction and use of loop diuretics. 2.1gm/dl. A 24 hr urinary protein revealed 4.2 Hemodialysis was initiated on day 10 of gms of protein with estimated creatinine hospitalization. At this time, the patients’s clearance of 2.7ml/min. A complete serological weight had climbed up to 75 kgs and he was work-up including serum complement C3,C4 mildly dysnoeic. He required a total of 15 litres ,antinuclear antibody, anticytoplasmic antibody , of ultra filtration before he was deemed to have anti HIV,HCV and hepatitis B antibody were achieved dry weight. Hemodialysis was negative. continued for 4 weeks. The proteinuria and renal A percutaneous renal biopsy was performed one functions slowly improved after 5-6 weeks of day after admission and this included a total of prednisone therapy and at the time of hemo - 15 glomeruli with no sclerosed glomeruli. The dialysis discontinuation, the endogenous Cr Cl glomeruli were normal in size and appearance was 15.7ml/min. The patient continues to be on on light microscopy with no focal or segmental steroid therapy at last follow-up at 3 months sclerosis and mild vascular intimal hyperplasia. with serum creatinine of 3.0 mg/dl and he is off The interstitial space revealed mild focal tubular dialysis. The last estimated 24 hr protein is injury, no tubular fibrosis or atrophy was noted. >1gm/day. A summary of relevant clinical data Immuno flouresence of the specimen revealed is presented in Table 1. Table1. Investigations of the patient Day of Urea(mg/dl) S.Creat(mg/dl) Serum K T.Protein Serum Urine Urine Cr Cl Weight of admission Albumin PCR Protein patient 1 67.9 1.6 - 4.5 2.1 3.2 4+ 35 67.0 5 143.6 2.66 6.3 70.5 7 166.8 3.57 5.2 17.7 74.5 10+ 195 4.63 4.7 14.7 75.8 14 101.6 4.71 4.5 0.94 14.3 68.5 20 9.0 5.8 5.7 57.5 24 7.2 7.2 58.3 28 7.3 4.4 2.4 4.29 7.3 58.6 Abbreviations: PCR –protein creatinine ratio Cr Cl: Creatinine clearance + Initiation of hemodialysis 2. DISCUSSION uncommon when compared to the classic presentation of nephrotic syndrome with The phenomenon of acute renal failure in preserved glomerular filtration rate (GFR). nephrotic syndrome with normal or near normal Information on the pathophysiology that structure was first described in detail by underlies acute renal failure has been varied and Chamberlain et al way back in 1966(7). This distinct. initial report described nine cases of oliguric renal failure occurring unexpectedly in the Since the first report by Chamberlain et al, many course of nephrotic syndrome though renal investigators have suggested that a reduction in pathology revealed a range of glomerular effective intravascular volume induced by a diseases. Since then several case reports and lower plasma oncotic pressure and interstitial case series have reported reversible acute renal fluid space seeping leads to a fall in GFR failure in patients presenting with nephrotic leading to renal dysfunction. However this syndrome with minimal change disease on renal pathophysiologic mechanism has not been histology(1,4-5,20,21). It is however relatively accepted by other investigators who have ARC Journal of Nephrology Page | 2 Revisiting Acute Kidney Injury in Minimal Change Disease- a Case Report and Review of Literature proposed different mechanisms. We review the As shown in Fig 1, other factors may affect current thinking on this entity. The major factors single nephron GFR in patients with nephrotic that regulate GFR are: circulating blood volume, syndrome. This could be a decrease in ▲P renal blood flow and the intrinsic determinants (transcapillary hydraulic pressure) due to an of single nephron GFR. increase in Pf (tubular hydrostatic pressure), primary reduction in Kf (ultrafiltration co- Blood Volume in nephrotic syndrome: The efficient), either by a reduction in the traditional view of the pathogenesis of oedema glomerular surface available for filtration or by formation in the nephrotic syndrome was that an change in glomerular water permeability or low plasma oncotic pressure resulting from both. hypoalbuminaemia would activate Starlings’ forces favouring transudation of plasma fluid into the interstitial space. The resulting decrease in effective intravascular circulating volume would then trigger volume-regulatorysensors to cause sodium and water retention by the kidneys. This view was however challenged by Eisenberg in 1968 who demonstrated that blood volume was normal in edematous nephrotic syndrome patients (8). Other subsequent studies have also supported Eisenberg’s hypothesis that with certain exceptions, no demonstrable difference existed between circulating blood /plasma volume in nephrotic and normal Fig1: Representation of glomerular pressure individuals (9, 10). However observations of gradient normal volumes should not be taken as proof that minor degrees of hypovolemia do not exist.
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