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BACKGROUND Minimal change disease is a common cause of nephrotic syndrome in adults. There are few reported cases of vaccine-related podocytopathy with nephrotic-range proteinuria in the setting of a minimal change disease history. There have been rare reports of acute renal damage following vaccination to prevent COVID-19 and some cases of exacerbation of ongoing nephropathy. This report is a 33-year-old man with a 22-year history of nephrotic syndrome due to minimal change disease which exacerbated following a third dose of an mRNA SARS-CoV-2 vaccine for COVID-19. CASE REPORT We report a case of nephrotic syndrome after the third dose of the BNT162b2 mRNA COVID-19 vaccine. The patient presented with mild edema in the bilateral lower extremities and sacrum. Laboratory investigations confirmed nephrotic-range proteinuria and hypoalbuminemia. A kidney sonogram demonstrated mild renal parenchymal disease and a small non-obstructing right renal calculus. Renal biopsy revealed diffuse podocyte foot process effacement, punctuate IgG podocyte cytoplasmic staining, and minimal global glomerulosclerosis, consistent with a diagnosis of a diffuse podocytopathy with a minimal change disease phenotype. The patient was started on oral prednisone treatment, which led to remission of his symptoms and normalization of lab test results with normal BUN and Cr and resolution of proteinuria. Treatment was tapered off over the course of 28 weeks. CONCLUSIONS We presents a case of longstanding minimal change disease that showed exacerbation following a third dose of an mRNA vaccine for SARS-CoV-2. Although this may be a rare association, this case supports that patients with chronic glomerulonephritis need to be monitored.

A 70-year-old female patient developed acute interstitial nephritis (AIN) after treatment with non-steroidal anti-inflammatory drugs (NSAIDs), proton pump inhibitors (PPI), and Bromhexine. Renal biopsy confirmed the diagnosis, and the patient was treated with oral prednisone. Careful attention to timing of acute kidney injury (AKI) is crucial to diagnosing AIN.

Polycystic kidney disease (PKD) is a multiorgan disorder resulting in fluid-filled cyst formation in the kidneys and other systems. The replacement of kidney parenchyma with an ever-increasing volume of cysts eventually leads to kidney failure. Recently, increased understanding of the pathophysiology of PKD and genetic advances have led to new approaches of treatment targeting physiologic pathways, which has been proven to slow the progression of certain types of the disease. We review the pathophysiologic patterns and recent advances in the clinical pharmacotherapy of autosomal dominant PKD. A multipronged approach with pharmacologic and nonpharmacologic treatments can be successfully used to slow down the rate of progression of autosomal dominant PKD to kidney failure.

Rationale & objectiveEuvolemic hyponatremia often occurs due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Vasopressin 2 receptor antagonists may be used to treat SIADH. Several of the major trials used 15 mg of tolvaptan as the lowest effective dose in euvolemic and hypervolemic hyponatremia. However, a recent observational study suggested an elevated risk for serum sodium level overcorrection with 15 mg of tolvaptan in patients with SIADH.Study designA retrospective chart review study comparing outcomes in patients with SIADH treated with 15 versus 7.5 mg of tolvaptan.Settings & participantsPatients with SIADH who were treated with a very low dose of tolvaptan (7.5 mg) at a single center compared with patients using a 15-mg dose from patient-level data from the observational study described previously.PredictorsTolvaptan dose of 7.5 versus 15 mg daily.OutcomesAppropriate response to tolvaptan, defined as an initial increase in serum sodium level > 3 mEq/L, and overcorrection of serum sodium level (>8 mEq/L per day, and >10 mEq/L per day in sensitivity analyses).Analytical approachDescriptive study with additional outcomes compared using t tests and F-tests (Fischer's Exact χ2 Test).ResultsAmong 18 patients receiving 7.5 mg of tolvaptan, the mean rate of correction was 5.6 ± 3.1 mEq/L per day and 2 (11.1%) patients corrected their serum sodium levels by >8 mEq/L per day, with 1 of these increasing by >12 mEq/L per day. Of those receiving tolvaptan 7.5 mg, 14 had efficacy, with increases ≥ 3 mEq/L; similar results were seen with the 15-mg dose (21 of 28). There was a statistically significant higher chance of overcorrection with the use of 15 versus 7.5 mg of tolvaptan (11 of 28 vs 2 of 18; P = 0.05; and 10 of 28 vs 1 of 18; P = 0.03, for >8 mEq/L per day and >10 mEq/L per day, respectively).LimitationsSmall sample size, retrospective, and nonrandomized.ConclusionsTolvaptan, 7.5 mg, daily corrects hyponatremia with similar efficacy and less risk for overcorrection in patients with SIADH versus 15 mg of tolvaptan.

Hepatitis C (HCV) infection has a prevalence of 3 million infected individuals in the United States, according to recent Center for Disease Control reports, and can have various renal manifestations. Cryoglobulins, antibodies that precipitate at colder temperatures in vitro, are a relatively common cause of renal disease in HCV infection. The cryoglobulin proteins can form occlusive aggregates in small glomerular capillary lumina or deposit in other areas of the glomerulus, resulting in hypocomplementemia, proteinuria, hematuria, and renal injury. The typical biopsy pattern is that of membranoproliferative glomerulonephritis (MPGN). There are, however, other HCV-related patterns of glomerular injury. Anti-neutrophil cytoplasmic antibodies (ANCA) are known to exist in HCV-infected patients. In many reported cases, ANCA serologic testing may appear positive due to cross-reactivity of the immune assays; however, the biopsy findings do not support ANCA-associated crescentic glomerulonephritis (GN)/vasculitis as the primary cause of glomerular injury. There are rare reports of microscopic polyangiitis (MPA) p-ANCA vasculitis, in patients with HCV infection. In comparison with the MPGN pattern of cryoglobulinemic glomerular injury, biopsies from these HCV-infected patients with concomitant MPA revealed a crescentic GN, associated with normal serum complement levels. We present a case of HCV-associated glomerular disease with the surprising biopsy finding of necrotizing and crescentic p-ANCA GN, with a background, low-grade mesangial immune complex GN. Thus, p-ANCA disease should also be considered in HCV-infected patients, in addition to the more typical lesions of MPGN or cryoglobulinemic GN.

BACKGROUND Minimal change disease is a common cause of nephrotic syndrome in adults. There are few reported cases of vaccine-related podocytopathy with nephrotic-range proteinuria in the setting of a minimal change disease history. There have been rare reports of acute renal damage following vaccination to prevent COVID-19 and some cases of exacerbation of ongoing nephropathy. This report is a 33-year-old man with a 22-year history of nephrotic syndrome due to minimal change disease which exacerbated following a third dose of an mRNA SARS-CoV-2 vaccine for COVID-19. CASE REPORT We report a case of nephrotic syndrome after the third dose of the BNT162b2 mRNA COVID-19 vaccine. The patient presented with mild edema in the bilateral lower extremities and sacrum. Laboratory investigations confirmed nephrotic-range proteinuria and hypoalbuminemia. A kidney sonogram demonstrated mild renal parenchymal disease and a small non-obstructing right renal calculus. Renal biopsy revealed diffuse podocyte foot process effacement, punctuate IgG podocyte cytoplasmic staining, and minimal global glomerulosclerosis, consistent with a diagnosis of a diffuse podocytopathy with a minimal change disease phenotype. The patient was started on oral prednisone treatment, which led to remission of his symptoms and normalization of lab test results with normal BUN and Cr and resolution of proteinuria. Treatment was tapered off over the course of 28 weeks. CONCLUSIONS We presents a case of longstanding minimal change disease that showed exacerbation following a third dose of an mRNA vaccine for SARS-CoV-2. Although this may be a rare association, this case supports that patients with chronic glomerulonephritis need to be monitored.

Rationale & Objective: Euvolemic hyponatremia often occurs due to the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Vasopressin 2 receptor antagonists may be used to treat SIADH. Several of the major trials used 15 mg of tolvaptan as the lowest effective dose in euvolemic and hypervolemic hyponatremia. However, a recent observational study suggested an elevated risk for serum sodium level overcorrection with 15 mg of tolvaptan in patients with SIADH., Study Design: A retrospective chart review study comparing outcomes in patients with SIADH treated with 15 versus 7.5 mg of tolvaptan., Settings & Participants: Patients with SIADH who were treated with a very low dose of tolvaptan (7.5 mg) at a single center compared with patients using a 15-mg dose from patient-level data from the observational study described previously., Predictors: Tolvaptan dose of 7.5 versus 15 mg daily., Outcomes: Appropriate response to tolvaptan, defined as an initial increase in serum sodium level > 3 mEq/L, and overcorrection of serum sodium level (>8 mEq/L per day, and >10 mEq/L per day in sensitivity analyses)., Analytical Approach: Descriptive study with additional outcomes compared using t tests and F-tests (Fischer's Exact χ2 Test)., Results: Among 18 patients receiving 7.5 mg of tolvaptan, the mean rate of correction was 5.6 ± 3.1 mEq/L per day and 2 (11.1%) patients corrected their serum sodium levels by >8 mEq/L per day, with 1 of these increasing by >12 mEq/L per day. Of those receiving tolvaptan 7.5 mg, 14 had efficacy, with increases ≥ 3 mEq/L; similar results were seen with the 15-mg dose (21 of 28). There was a statistically significant higher chance of overcorrection with the use of 15 versus 7.5 mg of tolvaptan (11 of 28 vs 2 of 18; P  = 0.05; and 10 of 28 vs 1 of 18; P  = 0.03, for >8 mEq/L per day and >10 mEq/L per day, respectively)., Limitations: Small sample size, retrospective, and nonrandomized., Conclusions: Tolvaptan, 7.5 mg, daily corrects hyponatremia with similar efficacy and less risk for overcorrection in patients with SIADH versus 15 mg of tolvaptan., (© 2019 The Authors.)