Hypokalaemia-induced acute renal failure
Hypokalaemia-induced acute renal failure
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DOI：
10.1093/ndt/14.9.2216
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发表时间：
1999-09-01
影响因子：
6.1
通讯作者：
Thomson, NM
中科院分区：
文献类型：
--
作者：
Menahem, SA;Perry, GJ;Thomson, NM
2 29 mmHg, PO 2 Potassium deficiency alters the function of several 96 mmHg, bicarbonate 13 mmol/l, oxygen saturation organs and most predominantly affects the cardiovas-98%. Serum glucose, amylase and lactate were within cular system, neurological system, muscles and kidneys normal limits. Serum calcium was 2.19 mmol/l, mag-[1]. Cardiac complications of prolonged hypokalaemia nesium 1.05 mmol/l and phosphate 3.57 mmol/l. include ventricular arrhythmias and hypertension. Creatinekinasewas300U/l (normal< 200 U/l). Total Neuromuscular manifestations include muscle weak-protein was 70 g/l, albumin was 34g/l, other liver ness and cramps as well as an increased incidence of function tests were within normal limits. Full rhabdomyolysis. The described renal lesions associated blood examination revealed a Hb of 17 g/dl, with chronic hypokalaemia include: proximal tubular WCC 14.04× 109/l, neutrophils 12.29× 109/l, platelets vacuolization accompanied by nephrogenic diabetes 239× 109/l. INR (international normalized ratio for insipidus [2], interstitial nephritis accompanied by prothrombintime) was2. 6andAPTT (activatedpartial varying degrees of renal impairment [3, 4] and an thromboplastin time) 44.2 s. ECG revealed sinus increased incidence of simple renal cysts [5]. We report rhythm with a left axis deviation, T-wave flattening a case of reversible anuric acute renal failure arising but no U waves. Renal ultrasound showed normal in a patient with known chronic hypokalaemia second-sized kidneys with no evidence of hydronephrosis. ary to prolonged laxative abuse. Serum electrolytes and renal function tests had been performed on the patient 3 and 5 years prior to this presentation. These showed normal serum sodium,
