Nephrotic syndrome complicated by tubular dysfunction. Case report and review of possible mechanisms

Luder, Anthony; Cohen, Simon; Fisher, Corinne

doi:10.1136/pgmj.56.654.282

Cited by 1 publication

(1 citation statement)

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“…The association between nephrotic syndrome and hypokalemia was also discussed to elucidate the molecular pathogenesis and its clinical relevance. The association between hypokalemia and nephrotic syndrome has been discussed since 1980’s [ 8 ]. Yamaguichi demonstrated a case of membranous GN patient with the hypokalemic presentation, and Liddle’s syndrome-like pattern, which had hypertension with or without metabolic alkalosis (Pagani L, et al, Hypertension.…”

Section: Discussionmentioning

confidence: 99%

The exacerbated hypokalemia in membranous glomerulonephritis due to proximal tubular injury: a neglect issue from a case report and literature review

Chang¹,

Hou

2023

BMC Nephrol

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Background Membranous glomerulonephritis is the most common primary etiology for the nephrotic syndrome in adults. Beyond the clinical hallmark of nephrotic syndrome such as fluid overloading, dyslipidemia and hypoalbuminemia, the dysregulated homeostasis of potassium and its possible mechanism is seldomly discussed, and its association with the clinical course of membranous GN is lacking. Case presentation A 65 year-old female attended to our emergent department for progressive lower leg edema after taking 15-h of flight. Hypoalbuminemia and hyperlipidemia were both noted, and 24-h urinary total protein was up to 17,950 mg/day. Elevated creatin-phospho-kinase developed at the initial presentation with hypokalemia due to excressive renal excretion. Glycosuria without elevated glycated Hemoglobin occurred. The pathology of kidney biopsy revealed subepithelial immunocomplex deposits with spike formation in the electron microscopy and the positive anti-Phosphlipase A2 receptor antibodies(PLA-2R) with hallmark of membranous glomerulonephritis. In the light microscopy, the vacuolization of proximal tubules was noted, which contributed to the potassium wasting. After 1 year following up duration, the patient’s proteinuria persisted after maintenance treatment with calcineurin inhibitor. Conclusion Hypokalemia is a neglected issue in the membranous glomerulonephritis. Unlike the previous literature, our patient had the vacuolization of proximal tubule at the initial presentation with hypokalemia, which might contribute the potassium wasting. The proximal tubular damage with hypokalemia might be a predictive factor for membranous glomerulonephritis.

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Section: Discussionmentioning

confidence: 99%