HYPOKALEMIC NEPHROPATHY IN NEPHROTICSYNDROME PATIENT

Introduction:Hypokalemic nephropathy (HN) caused by prolonged K+deficiency is associated with metabolic alkalosis, polydipsia, polyuria,growth retardation, hypertension, and progressive tubulointerstitialinjury. Histopahologic report of HN in nephrotic syndrome (NS) patientis rare.Methods:A 27 year male sufferedfrom weakness,especially lower leg,sincetwoweekspriortoadmission.ThepatientshadahistoryofNSsincechildhood and cared by nephrologist. Recent condition was hemody-namicallystable,laboratoryexaminationshowedpotassiumserum1.85mmol/L, albumin plasma 1.8 g/dL,serum creatinine 2.45 mg/dL, andmarked dyslipidemia. The patient was clinically assesed with hypo-kalemia, relapse nephroticsyndrome and renal insufficiency. Intrave-nous potassium was given and renal biopsy was performed.Histopathologicfindingsshowedglobalsclerosis.Thespecificfindingsmay related to HN were mesangial proliferation and specificlesionsontubules including athrophy, vacuolization, intratubular deposition ofamorphous and laminated hyaline materials and colloidisation oftubularepithelial,andinterstitialnephritis.Thepatientwasdischargedat 10thday of hospitalization with potassium level 2.93 mmol/L, andserum creatinine 1.95 mg/dL. The patient was treated with oral meth-ylprednisolone, mychophenolate mofetil, ACE-inhibitor, simvastatinand oral potassiumResults:Hypokalemic nephropathy may associate with chronichypokalemia. Hypokalemia, especially if persistently occurs, caninduce a variety of changes in renal tissue, impairing tubulartransport and possibly inducing chronic tubulointerstitial diseaseand cyst formation. HN also associated with alterations inintrarenal vasoactive substances, leading to vasoconstriction, salt-sensitivity, and progression of interstitialfibrosis. Histopatho-logical changes in HN, including severe tubular dilatation,intratubular deposition of amorphous and laminated hyaline ma-terials, intratubular cellular casts, and tubular atrophy is found.Moreattentionispaidtoathrophyandvacuolarchangesinrenaltubular epithelium accompanied by inflammatory interstitialchanges in patients with potassium losses. One function that isnot impaired is the ability to appropriately conserve potassium,which can be important in distinguishing between extrarenal andrenal sources of potassium losses when the cause of hypokalemiais not clear.