Abstract

Acute kidney injury in the context of nephrotic syndrome is a serious and alarming clinical problem. Largely, acute kidney injury is a relatively frequent complication among patients with comorbidities while it has been independently associated with an increased risk of adverse outcomes, including death and chronic kidney disease. Nephrotic syndrome, without hematuria or with minimal hematuria, includes a list of certain glomerulopathies; minimal change disease, focal segmental glomerulosclerosis and membranous nephropathy. In the light of primary nephrotic syndrome, pathophysiology of acute kidney injury is differentiated by the nature of the primary disease and the severity of the nephrotic state. This review aims to explore the clinical circumstances and pathogenetic mechanisms of acute kidney injury in patients with nephrotic syndrome due to primary glomerulopathies, focusing on newer perceptions regarding the pathogenesis and management of this complicated condition, for the prompt recognition and timely initiation of appropriate treatment in order to restore renal function to its baseline level. Prompt recognition of the precise cause of acute kidney injury is crucial for renal recovery. Clinical characteristics, laboratory and serological findings along with histopathological findings, if required, will reveal the implicated pathway leading to individualized approach and management.

Highlights

  • Acute kidney injury (AKI), in the context of nephrotic syndrome (NS), is a serious and alarming clinical problem

  • AKI is frequent among patients with comorbidities, while it has been correlated with an increased frequency of adverse outcomes, including death [1,2,3], and chronic renal failure [4]

  • According to the Kidney Disease Improving Global Outcomes (KDIGO) [9] definition, AKI is characterized by an increase in serum creatinine by ≥0.3 mg/dL within

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Summary

Introduction

Acute kidney injury (AKI), in the context of nephrotic syndrome (NS), is a serious and alarming clinical problem. AKI is frequent among patients with comorbidities, while it has been correlated with an increased frequency of adverse outcomes, including death [1,2,3], and chronic renal failure [4]. The risk of developing end stage kidney disease has been reported to increase. Acute kidney injury is classified by the main pathophysiologic mechanism involved in prerenal, intrinsic renal and postrenal causes. Any of these scenarios may occur in patients with NS due to primary glomerulopathy, the prerenal and intrinsic ones are the most frequent seen in this setting. This review aims to explore the clinical circumstances and pathogenetic mechanisms of AKI in patients with NS, focusing on newer perceptions regarding the pathogenesis and management of this complicated condition, for the prompt recognition and timely initiation of appropriate treatment in order to restore renal function to its baseline level

Definitions and Epidemiology of AKI
Frequency of AKI in Patients with NS
Pathophysiology of NS
Acute Tubular Necrosis
Acute Interstitial Nephritis
Renal Vein Thrombosis
Aggressive Disease
Crescentic Glomerulonephritis Superimposition
Calcineurin Inhibitors Toxicity
Management of Patients with AKI in Patients with NS
Findings
Algorithm patientswith withAKI
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