Aged ; Electrocardiography ; Female ; Humans ; Hyperkalemia ; complications ; physiopathology ; Myocardial Ischemia ; etiology

Humans ; Hyperkalemia ; etiology ; Male ; Middle Aged ; Postoperative Complications ; etiology ; Primary Myelofibrosis ; etiology ; Splenectomy ; adverse effects

A 49-year-old man with liver cirrhosis and hypertension was found to have hyperkalemia out of a degree of renal insufficiency and metabolic acidosis with low to normal anion gap, aggravated by volume contraction with diarrhea and medications (captopril, spironolactone and atenolol) interfering with potassium homeostasis. Plasma renin activity and serum aldosterone levels of this patient on a regular diet after discontinuation of medications were very low compared to those of five other cirrhotic patients with normokalemia as controls. Also, the renin-aldosterone stimulation testing on this patient performed by sodium restricted diet and furosemide, upright position and by angiotensin converting enzyme inhibition (captopril, 50 mg) showed the blunted renin and aldosterone responses to each of these stimuli, almost no changes from baseline renin and aldosterone levels, it was concluded that the underlying defect responsible for hyperkalemia in this case was hyporeninemic hypoaldosteronism and this was aggravated by other factors or drugs affecting potassium homeostasis.
Aldosterone/blood ; Captopril/pharmacology ; Furosemide/pharmacology ; Humans ; Hyperkalemia/*etiology ; Hypertension/*complications ; Hypoaldosteronism/*complications ; Liver Cirrhosis/*complications ; Male ; Middle Aged ; Renin/blood

This study was aimed at investigating the mechanisms of clinically important overt hyperkalemia in diabetes mellitus with underlying hyporeninemic hypoaldosteronism known as a classic model of the syndrome of hyporeninemic hypoaldosteronism (SHH). Rats (Sprague-Dawley, male) were streptozotocin-treated (60 mg/kg, ip) and used after 60 days. Rats with plasma glucose levels higher than 300 mg/dL (mean +/- SEM, 423 +/- 20 mg/dL, n = 8) were selected as the diabetic group. Age-matched normal rats served as control (mean plasma glucose, 88 +/- 2, mg/dL, n = 8). Serum potassium concentrations and osmolalities as well as serum creatinine levels were significantly higher in the diabetic than in the control group (5.07 +/- 0.09 vs. 4.68 +/- 0.11 mEq/L; 330 +/- 14 vs 290 +/- 3 mOsm/L; 0.40 +/- 0.03 vs 0.31 +/- 0.02 mg/dL, p < 0.05). Plasma renin activity (PRA) in the diabetic group was significantly lower than that in the control group (6.0 +/- 1.0 vs 12.1 +/- 1.1 ng Al/ml/h, p < 0.001). Plasma aldosterone concentration (PAC) was also significantly lower in the former than in the latter (368 +/- 30 vs 761 +/- 57 pg/ml, p < 0.001). Renomegaly, abnormal distal tubular cells with few organelles, and increased lipid droplets with pyknotic nucleus in zona glomerulosa of the adrenal glands were noted in the diabetic group. In conclusion, multifactorial causes including insulinopenia, hyperosmolality, elevated serum creatinine level and hypoaldosteronism with possible contribution of altered distal tubular response to aldosterone may have interacted to develop hyperkalemia in these diabetic rats.
Animals ; Diabetes Mellitus, Experimental/blood/*complications/pathology ; Disease Models, Animal ; Hyperkalemia/*complications ; Hypoaldosteronism/*complications ; Kidney Tubules, Distal/ultrastructure ; Male ; Rats ; Rats, Sprague-Dawley ; Reference Values ; Zona Glomerulosa/ultrastructure

Type 1 myotonic dystrophy (DM1) is an autosomal-dominant inherited disorder with a multisystem involvement, caused by an abnormal expansion of the CTG sequence of the dystrophic myotonia protein kinase (DMPK) gene. DM1 is a variable multisystem disorder with muscular and nonmuscular abnormalities. Increasingly, endocrine abnormalities, such as gonadal, pancreatic, and adrenal dysfunction are being reported. But, Electrolytes imbalance is a very rare condition in patients with DM1 yet. Herein we present a 42-yr-old Korean male of DM1 with abnormally elevated serum sodium and potassium. The patient had minimum volume of maximally concentrated urine without water loss. It was only cured by normal saline hydration. The cause of hypernatremia was considered by primary hypodipsia. Hyperkalemic conditions such as renal failure, pseudohyperkalemia, cortisol deficiency and hyperkalemic periodic paralysis were excluded. Further endocrine evaluation suggested selective hyperreninemic hypoaldosteronism as a cause of hyperkalemia.
Adult ; Humans ; Hyperkalemia/complications/*diagnosis ; Hypernatremia/complications/*diagnosis ; Hypoaldosteronism/complications/diagnosis ; Kidney Concentrating Ability ; Male ; Myotonic Dystrophy/complications/*diagnosis/*genetics ; Potassium/blood ; Protein-Serine-Threonine Kinases/*genetics ; Sodium/blood

Colonic necrosis is known as a rare complication following the administration of Kayexalate (sodium polystryrene sulfonate) in sorbitol. We report a rare case of colonic mucosal necrosis following Kalimate (calcium polystryrene sulfonate), an analogue of Kayexalate without sorbitol in a 34-yr-old man. He had a history of hypertension and uremia. During the management of intracranial hemorrhage, hyperkalemia developed. Kalimate was administered orally and as an enema suspended in 20% dextrose water to treat hyperkalemia. Two days after administration of Kalimate enema, he had profuse hematochezia, and a sigmoidoscopy showed diffuse colonic mucosal necrosis in the rectum and sigmoid colon. Microscopic examination of random colonic biopsies by two consecutive sigmoidoscopies revealed angulated crystals with a characteristic crystalline mosaic pattern on the ulcerated mucosa, which were consistent with Kayexalate crystals. Hematochezia subsided with conservative treatment after a discontinuance of Kalimate administration.
Adult ; Colon/*pathology ; Gastrointestinal Hemorrhage/etiology ; Humans ; Hyperkalemia/drug therapy ; Intestinal Mucosa/*pathology ; Male ; Necrosis/*chemically induced/complications/pathology ; Polystyrenes/*adverse effects/therapeutic use ; Uremia/*physiopathology

Patients with autosomal dominant polycystic kidney disease have significant morbidity due to large kidney size. Surgical extirpation of polycystic kidneys is frequently necessary to treat the morbidity or to obtain intraabdominal space for a graft kidney. Simultaneous bilateral nephrectomy and kidney transplantation are performed in many transplant centers to avoid the complications associated with anephric states such as anemia requiring blood transfusion, osteodystrophy, fluid overload, hyperkalemia, and congestive heart failure. However, the risk of postoperative complications after combined bilateral nephrectomy with kidney transplantation is relatively high, especially for cases in which the polycystic kidneys are huge. Here, we report two cases of severe and persistent hypotension during and after combined surgery which may have been caused by adrenal insufficiency or by sympathetic denervation and splanchnic vasculature decompression after the removal of huge polycystic kidneys.
Adrenal Insufficiency ; Anemia ; Blood Transfusion ; Decompression ; Heart Failure ; Humans ; Hyperkalemia ; Hypotension* ; Kidney Failure, Chronic* ; Kidney Transplantation* ; Kidney* ; Nephrectomy* ; Polycystic Kidney Diseases* ; Polycystic Kidney, Autosomal Dominant ; Postoperative Complications ; Sympathectomy ; Transplants

One hundred sixty-three patients with graded degrees of uncomplicated stable chronic renal failure were studied to investigate the quantitative relationship between serum acid-base and electrolyte composition and serum creatinine level. Even in patients with a mild degree of renal failure, the serum total carbon dioxide (tCO2) content was reduced significantly. Progressive decrements in tCO2 were noted in the more severe degrees of renal failure with the reciprocal relationship between tCO2 and serum creatinine concentration. Depending upon the degree of chronic renal failure, the type of metabolic acidosis was different. In patients with a moderate degree of renal failure, hyperchloremic acidosis was noted with anion gap remaining normal. As the renal failure progressed to a more severe degree, this pattern of hyperchloremic acidosis changed to anion gap acidosis with a normal serum chloride level. The highest anion gap was 25 mEq/L in the patient with serum creatinine concentration 24.7mg/dL.
Acid-Base Equilibrium* ; Acidosis/etiology* ; Adult ; Carbon Dioxide/blood ; Chlorides/blood ; Creatinine/blood ; Electrolytes/blood* ; Human ; Hyperkalemia/etiology ; Kidney Failure, Chronic/blood* ; Kidney Failure, Chronic/complications ; Middle Age ; Sodium/blood