Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Description of 23 patients (21 women, 2 men) with an average age of 36.6 (19--68) years, who were hypokalemic during 6.5 years on the average (range 1/2--16 years). The cause of the potassium depletion was malnutrition (anorexia nervosa, vomiting) and/or abuse of laxatives and/or diuretics. With increasing duration of potassium depletion renal function deteriorated; in two cases terminal renal failure developed. Histology of the kidneys (9 cases) showed the picture of chronic abacterial interstitial nephritis. Urinalysis was negative or non-specific. The blood pressure levels were normal or low, hypertensive values being exceptional. Aside of hypokalemia a tendency to hyponatriemia, hypochloremia and metabolic alcalosis was observed, the latter turning into hypokalemic normochloremic acidosis with advancing renal insufficiency. Plasma renin activity and aldosterone concentration or excretion frequently were elevated, but no close correlation was found between these parameters or with the blood pressure. Bacterial infection of the urinary tract occured, if at all, in the late phase and seems to be complication rather than the cause of the kidney disease. The discussion of other possible pathogenetic factors leads to the conclusion that the term "chronic kaliopenic nephropathy" is justified. Some diagnostic and therapeutic consequences are mentioned.
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PMID:Chronic hypokalemic nephropathy: a clinical study. 73 56

A 32-year-old man was diagnosed as having pseudo-Bartter syndrome due to surreptitious habitual vomiting and to maldigestion related to decayed teeth. His chief complaints were muscle pain and weakness. In this case, metabolic alkalosis, hypokalemia, hypochloremia, increased plasma renin activity and aldosterone levels were noticed with marked decreases in urinary chloride excretion. Creatinine clearance (GFR) and renal plasma flow (RPF) were also decreased. Blood pressure was normal, but the pressor response to angiotensin II was attenuated. Before treatment with 0.9% saline infusion, plasma vasopressin (AVP) was not suppressed sufficiently by lowering the plasma osmolality (Posm) with an oral water load (WL), but it normally responded to a rise in Posm due to hypertonic saline infusion. Moreover, plasma AVP was normally suppressed by WL after the replenishment of saline. Plasma atrial natriuretic peptide (ANP) was low before WL, but increased normally in response to WL. However, inconsistent with the normal response in this case, decreases in plasma AVP failed to dilute urinary osmolality and to increase urine flow, irrespective of the levels of plasma ANP. These results indicate that chronic inanition due to surreptitious vomiting causes impaired renal diluting ability through decreases in GFR and RPF, irrespective of the levels of plasma AVP and ANP.
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PMID:Impaired water diuresis in a patient with pseudo-Bartter syndrome. 153 41

Plasma renin activity (PRA) and plasma angiotensin II (PAT II) level were determined with the method of radioimmunoassay in 55 patients with advanced chronic obstructive pulmonary disease (COPD) and chronic cor pulmonale (41 of them had respiratory failure) and 12 healthy aged persons. The results showed that PRA and PAT II levels were significantly elevated in the presence of such factors as severe hypoxia and hypercapnia (PaO2 less than or equal to 45 mmHg, mean 40 mmHg, PaCO2 greater than or equal to 65 mmHg), right heart failure, acidosis, hyponatremia and hypochloremia. It is shown that the prognosis would be poor when the patient's PRA level is significantly elevated.
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PMID:[Influence of acute respiratory failure on plasma renin activity and plasma angiotensin II level in advanced chronic obstructive pulmonary disease and chronic cor pulmonale]. 268 74

We have suggested that the renal tubular signal for renin release is related to alterations of sodium chloride cotransport in the TALH. Renin release is inhibited by increased sodium chloride transport and stimulated by interrupted sodium chloride transport. Because of the different affinities of the carriers for sodium and chloride, chloride rather than sodium is rate limiting for this cotransport process. Consequently, renin release is related to alterations of chloride delivery rather than sodium delivery to the TALH. The reduction of PRA by selective chloride loading and by short-term infusion of chloride salts is related to increased chloride delivery to the loop and hence increased chloride transport. Alternatively, chlorpropamide and antidiuretic hormone may inhibit renin release by increasing chloride delivery to the loop. Stimulation of renin release may likewise be related either to decreased chloride delivery and hence decreased transport in the loop (hypochloremia related to selective chloride deprivation) or to an intrinsic alteration in the transporting capacity of the loop (loop diuretics, potassium depletion, glucocorticoid deficiency, Bartter's syndrome). The intermediate steps between alterations of sodium chloride transport in the TALH and renin release remain to be defined.
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PMID:Renal tubular chloride and renin release. 331 41

K+ depletion of two kinds was induced in two groups of rats by selective dietary restriction for up to 5 weeks. Complete metabolic studies for H+, K+, Na+ and Cl- were carried out daily during weeks 1, 3 and 5. In control rats of group A (receiving K+ with sodium chloride), plasma pH (7.47) and HCO3- (25 mmol/l), as well TA (titratable acid)--HCO3- and NH+4 urinary excretion rates, were stable, while balances were nil for K+ and slightly positive for Cl-. In K+-deprived rats of group A receiving sodium chloride, a progressive metabolic alkalosis developed (plasma pH reached 7.57 and HCO3- 35.8 mmol/l by 5 weeks), and TA--HCO3- and NH+4 urinary excretion rates were not different from controls. Plasma K+ fell progressively from 4.20 to 2.20 mmol/l, with negative K+ balance. Balances for Na+ and H2O were highly positive and plasma renin activity and aldosterone decreased by week 5. Hypochloraemia developed with positive Cl- balance. In control rats of group B (receiving K+ with neutral sodium phosphate), a slight metabolic alkalosis developed, and TA--HCO3- excretion rate was increased compared with control rats of group A.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Selective dietary potassium depletion and acid-base equilibrium in the rat. 391 25

Acute laminitis-hypertension was produced by carbohydrate overloading of the gastrointestinal tract in 12 adult horses. Obel grade 3 (OG3) lameness developed 40 hours (+/- 3.5, SEM) after overfeeding. At OG3 lameness, mean plasma volume was significantly decreased (P less than 0.005) when compared with base-line values. Before OG3 lameness, transient decreases in serum phosphorus and calcium were recorded. Mild hyponatremia also developed before OG3 lameness and persisted. After establishment of OG3 lameness, persistent hypokalemia and increased plasma aldosterone concentration occurred coincidently. Transient increase in plasma hydrocortisone (cortisol) and renin activity and transient hypochloremia were also recorded during the syndromal phase. Changes in plasma volume and serum electrolytes are discussed and related to the pathogenesis of acute equine laminitis. The alterations in plasma renin activity and aldosterone concentration were interpreted as homeostatic adjustments to fluid and electrolyte imbalances. Differences between the horse and pony during onset of experimental alimentary laminitis are also discussed.
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PMID:Plasma volume, electrolyte, and endocrine changes during onset of laminitis hypertension in horses. 675 27

Hypochloremia has been associated by inference from clearance studies with disturbances in free water reabsorption and renal renin release by a macula densa mechanism. To examine directly these relationships, we studied chloride, fluid, and solute transport in the loop segment (LS) of rat superficial nephrons by micropuncture techniques following acute volume expansion with 0.15 m sodium chloride (CVE) or sodium bicarbonate (BVE). Plasma renin activity was suppressed in group CVE but not in group BVE. Blood pressure, plasma volume expansion, whole kidney GFR, urinary sodium excretion, late proximal and early distal SNGFR, and fluid delivery to the LS were no different between groups CVE and BVE despite different plasma chloride concentrations (102 +/- 5 mEq/liter for CVE vs. 74 +/- 3 for BVE; P less than 0.001). Absolute LS chloride reabsorption was less in BVE than it was in CVE (2030 +/- 120 pEq/min vs. 2454 +/- 136; P less than 0.025). This was associated with significantly lower fractional absolute LS solute reabsorption and higher early distal tubule fluid osmolality. These data demonstrate directly and in vivo that a decrease in chloride reabsorption in the LS of superficial nephrons is associated with impaired solute reabsorption in that segment and a failure to suppress plasma renin activity by sodium loading.
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PMID:Effect of hypochloremia on loop segment chloride and solute reabsorption in the rat during volume expansion. 704 92

Thirteen infants, 2 to 10 months of age, developed hypochloremic alkalosis (serum chloride 59 to 92 mEq/l) while taking Neo-Mull-Soy (Syntex), a soy-based formula low in chloride (measured to be 0 to 2 mEq/l) but with considerable potassium citrate. Range of symptoms included lethargy, anorexia, mild spitting up, diarrhea, hematuria, and growth failure. Urine chloride excretion was less than 3 mEq/l. Plasma renin activity or aldosterone, measured in six infants, was elevated. All responded promptly to supplemental salt. One infant receiving Neo-Mull-Soy redeveloped alkalosis when supplemental salt was discontinued. Two of nine apparently normal infants receiving Neo-Mull-Soy also had hypochloremia (85, 86 mEq/l). Three of four receiving Prosobee (Mead Johnson; Cl content 7 mEq/l) had urine chloride concentration less than 20 mEq/l. The chloride content of some infant formulas is insufficient to offset salt losses following mild stress.
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PMID:Hypochloremic alkalosis in infants associated with soy protein formula. 718 58

We report a 2 month-old infant referred for failure to thrive. At birth, weight was 3820 g and length 52 cm. After physiologic weight loss, the patient showed no further weight gain for the next two months. On admittance (age 2 mo), weight was 3340 g and length 53 cm; the infant had severe dystrophy, generalized hypotonia and dehydration; blood chemistry showed hyponatremia, hyperkalemia and hypochloremia. A salt losing syndrome of adrenal origin was hypothesized. However, rehydration and hydrocortisone administration failed to correct hyponatremia and hyperkalemia. Endocrine assessment showed high levels of aldosterone and plasma renin activity, suggesting pseudohypoaldosteronism. Oral sodium chloride supplementation normalized electrolyte balance and the patient showed progressive weight gain and catch-up growth, confirming the diagnosis.
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PMID:Pseudohypoaldosteronism: report of a case presenting as failure to thrive. 758

We report on a girl having congenital chloride diarrhea (CCD) who has been followed for 7 years and 6 months sequentially. Dilated intestinal loops, marked enlargement of the abdominal circumference of the fetus and hydramnios were noted by ultrasound examination at 31 weeks of gestation. After delivery by cesarean section for hydramnios, she excreted profuse watery yellow green stools with marked abdominal distension. At 4 months of age, hypochloremia, hyponatremia and a high concentration of chloride in the stool were identified. She was diagnosed as having CCD. Because it was difficult to administer a large volume of potassium chloride (KCl), and sodium chloride (NaCl), we decided to administer spironolactone. After administration of spironolactone, we could generate correct serum electrolytes using less amounts of KCl. At 7 years and 6 months of age, her body size was within normal limits and her intellectual, mental and physical development had been normal. In spite of normal serum electrolytes, blood pH and the presence of chloriduria, secondary hyperaldosteronism was noted. We consider that spironolactone may be useful to decrease the amount of KCl administration in the neonatal period, but frequent measurements of renin, angiotensin and aldosterone would be necessary for adequate control in CCD cases.
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PMID:A girl having congenital chloride diarrhea treated with spironolactone for seven years. 794 7


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