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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

IN TWO PATIENTS WITH CLASSIC RENAL TUBULAR ACIDOSIS (RTA) AND IN TWO PATIENTS WITH RTA ASSOCIATED WITH THE FANCONI SYNDROME, RENAL POTASSIUM WASTING PERSISTED DESPITE SUSTAINED CORRECTION OF ACIDOSIS: (a) during moderate degrees of hypokalemia, daily urinary excretion of potassium exceeded 80 mEq in each patient; (b) during more severe degrees of hypokalemia, daily urinary excretion of potassium exceeded 40 mEq in two patients and 100 mEq in another. These urinary excretion rates of potassium are more than twice those observed in potassium-depleted normal subjects with even minimal degrees of hypokalemia. The persistence of renal potassium wasting may have resulted in part from hyperaldosteronism, since urinary aldosterone was frankly increased in two patients and was probably abnormally high in the others relative to the degree of their potassium depletion. The hyperaldosteronism persisted despite sustained correction of acidosis, a normal sodium intake, and no reduction in measured plasma volume, and was not associated with hypertension; its cause was not defined. In the two patients with classic RTA, neither renal potassium wasting nor hyperaldosteronism could be explained as a consequence of a gradient restriction on renal H(+) - Na(+) exchange because the urinary pH remained greater than, or approximately equal to, the normal arterial pH or considerably greater than the minimal urinary pH attained during acidosis. The findings provide no support for the traditional view that renal potassium wasting in either classic RTA or RTA associated with the Fanconi syndrome is predictably corrected solely by sustained correction of acidosis with alkali therapy.
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PMID:Renal potassium wasting in renal tubular acidosis (RTA): its occurrence in types 1 and 2 RTA despite sustained correction of systemic acidosis. 510 85

Aldosterone deficiency is caused by various defects of aldosterone biosynthesis in the adrenal gland or hyporeninism. The most important symptoms are hyponatremia and hyperkalemia. These electrolyte disturbances are also found in pseudohypoaldosteronism. Pseudohypoaldosteronism type I is characterized by insensitivity of the distal nephron for aldosterone. Hyperabsorption of chloride in the distal nephron leads to pseudohypoaldosteronism type II, which is linked with hypertension, whereas blood pressure in the other mentioned disorders is decreased. Renal tubular acidosis, mainly type 4, with impaired production of ammonia due to hyperkalemia, is frequently observed in hypoaldosteronism and both types of pseudohypoaldosteronism as well. The therapeutic regimen is different: low doses of fludrocortisone in hypoaldosteronism, potassium restriction, sodium bicarbonate and loop diuretics in type I of pseudohypoaldosteronism, and sodium restriction and chloruretic diuretics (thiazide) in type II of pseudohypoaldosteronism. In some cases hyperkalemia requires the use of potassium-binding resins.
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PMID:[Primary hypoaldosteronism, pseudo-hypoaldosteronism and distal tubular acidosis]. 638 50

A 13-year-old white girl with severe hypertension and type IV renal tubular acidosis had decreased renal chloride clearance and exaggerated sodium chloride reabsorption by the ascending limb of Henle during hypotonic saline diuresis. Urinary prostaglandin E2 excretion was markedly diminished and often undetectable (0 to 37 ng/24 h). Treatment with oral furosemide completely reversed the hypertension and hyperkalemic acidosis, and effected a 20-fold rise in urinary prostaglandin E2. Sodium chloride reabsorption by the thick ascending limb of Henle decreased from 93.5% to 79.3%. Renal hypoprostaglandism may have a pathogenic role in this syndrome by enhancing chloride reabsorption in the ascending limb of Henle leading to extracellular fluid volume expansion, hypertension, and suppression of the renin-angiotensin-aldosterone axis. The therapeutic effects of furosemide may be partially mediated by enhancing the biosynthesis of renal prostaglandins or inhibiting their breakdown.
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PMID:Renal hypoprostaglandism, hypertension, and type IV renal tubular acidosis reversed by furosemide. 657 76

We studied the role of the renin-angiotensin system in the vasoconstrictor effect induced by prostaglandins (PG) on the renal microcirculation in 25 euvolemic Munich-Wistar rats. Infusions of subvasodepressor doses of PgE2 and PGI2 led to lower mean values for single nephron (SN) glomerular filtration rate (GFR), total kidney GFR, glomerular plasma flow rate, QA, and ultrafiltration coefficient (Kf) than were found in animals given vehicle alone (control group). On the other hand, the mean values for glomerular transcapillary hydraulic pressure difference, delta P, and total renal arteriolar resistance, RTA, tended to be higher in the experimental groups. The effects of PGI2 on the renal microcirculation were more pronounced than for PGE2. These increases in delta P and RTA and decreases in QA and Kf are typical of changes induced by angiotensin II (AII). To further explore this AII-like phenomenon, an infusion of saralasin, a competitive AII antagonist, was used. Indeed, when saralasin was infused together with either PGE 2 or PGI2 the previously noted effects on delta P, QA, RTA and Kf were largely abolished. Thus, saralasin transformed the renal action of PGE2 and PGI2 from vasoconstrictor (low QA, high RTA) to vasodilator (high QA and low RTA). Therefore, the effects of nonvasodepressor doses of PGE2 and PGI2 on the renal microcirculation appear to depend on an intermediate action of AII.
Hypertension
PMID:Possible mechanism of prostaglandin-induced renal vasoconstriction in the rat. 702 24

A 13-year-old girl with severe hypertension (240/140 mm Hg), short stature, marked hyperkalemia (8.6 mEq/liter), and renal tubular acidosis was studied. Renal parenchymal and renovascular diseases as well as endocrinologic causes of hypertension were ruled out by appropriate studies. The hypertension was associated with sodium retention, increased plasma volume, suppressed plasma renin activity, and decreased urinary excretion of aldosterone. Impaired renal excretion of potassium was demonstrated by sodium sulfate infusion when the patient was fed a high-sodium diet but a significant kaliuresis occurred when the test was performed on a low-sodium diet suggesting that renal sodium retention may play a role in the defect in potassium excretion. The renal tubular acidosis was associated with normal distal acidification but a low bicarbonate threshold (19 mmoles/liter) and marked suppression of urinary ammonium excretion. The hypertension, hyporeninemia, and hypoaldosteronism as well as the hyperkalemia and acid-base abnormalities were completely reversed by dietary sodium restriction or the administration of thiazides or furosemide. It is concluded that an unusual avidity for sodium chloride reabsorption by the renal tubules leading to extracellular volume expansion and renin-aldosterone suppression plays a significant pathogenic role in this syndrome and may explain the hypertension and biochemical abnormalities discussed.
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PMID:Severe hypertension, hyperkalemia, and renal tubular acidosis responding to dietary sodium restriction. 706 87

We report the eleventh case of granulomatous sarcoid nephritis and review the previous literature. Although not as commonly recognized as calcium nephropath, granulomatous nephritis may be an important cause of morbidity and mortality in patients with sarcoidosis. Its characteristics are similar to other tubulo-interstitial diseases. Mild to moderate albuminuria, microscopic hematuria and sterile pyuria predominate. Hypertension is usually absent and renal size is well preserved. Urinary concentration defects (including nephrogenic diabetes insipidus), renal tubular acidosis and inappropriate glucosuria may also be seen. Interstitial inflammation with non-caseating granulomas, epithelioid and multinucleated giant cells is the usual histologic picture. Intimal thickening is not infrequent and granulomas may occasionally involve the small arteries. Immunofluorescence and electron microscopic findings are non-specific.
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PMID:Granulomatous sarcoid nephritis: a cause of multiple renal tubular abnormalities. 742 93

The kidney is one of the organs susceptible to heavy metal intoxication. The total body burden and "saturation" level in renal tissue are important limiting factors to the onset of renal injuries. Acute or chronic exposure to many of heavy metals can induce renal tubulointerstitial injuries, including acute tubular necrosis, chronic tubulointerstitial nephritis, Fanconi syndrome, renal tubular acidosis, and renal tubular dysfunction without morphological changes. Chronic cadmium intoxication can cause irreversible Fanconi syndrome with chronic tubulointerstitial nephritis. Both urinary low-molecular weight protein excretion and urinary cadmium excretion (greater than 200-400 ppm) are the most reliable earlier markers of tubulointerstitial injury in chronic cadmium intoxication. The role of metallothionein is central to an understanding of cadmium-induced nephropathy. Acute lead intoxication in children can cause reversible Fanconi syndrome. Hypertension, hyperuricemia, and elevated serum creatinine, without Fanconi syndrome, are clinical manifestations of chronic lead exposure in adults. Nuclear inclusion body in proximal tubular cell is characteristic. Chronic exposure to inorganic germanium can cause chronic renal failure without urinary abnormalities, due to tubular degeneration and interstitial fibrosis, mainly in the thick ascending limb of Henle and distal tubulus.
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PMID:[Tubulointerstitial injuries in heavy metal intoxications]. 756 49

Glomerulopathy with predominant fibronectin deposits (GFD) is a newly recognized autosomal dominant renal disease that leads to albuminuria, microscopic hematuria, hypertension, renal tubular acidosis type IV, and end-stage renal disease in the second to fourth decade of life. Light microscopy documents extensive deposits in the subendothelial space, which on electron microscopy consist of non-oriented 12 x 125 nm fibers. Deposits are strongly immunoreactive for antibodies to fibronectin. We examined the hypothesis that a genetic defect in the gene for fibronectin is responsible for the disease. In a 197 member pedigree, 13 relatives developed end-stage renal failure from the disease. In 99 individuals haplotype analysis was performed using 6 microsatellite markers spanning a > 56 cM interval in chromosome region 2q34, where fibronectin, villin, and desmin map in close proximity. Haplotype analysis resulted in exclusion of the whole range of 78 cM covered by the markers examined. This result excludes fibronectin, villin, and desmin from being the causative genes for GFD in this large kindred.
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PMID:Glomerulopathy associated with predominant fibronectin deposits: exclusion of the genes for fibronectin, villin and desmin as causative genes. 872 29

In adults, persistent hyperkalemic distal renal tubular acidosis in the absence of impaired renal function is an unusual abnormality usually associated with the syndromes of aldosterone deficiency or resistance. Herein, we present an adult with a clinical picture consisting of a normal blood pressure of 125/80 mmHg, normal blood volume, and glomerular filtration rate, with hyperkalemic distal renal tubular acidosis. The patent could spontaneously lower her urine pH to less than 5.5. Plasma renin activity was normal. Serum aldosterone level was appropriately elevated for the level of serum potassium. Following alkalinization of the urine, she was able to generate a urinary to blood PCO2 gradient [U-B PCO2] of 55 mmHg, and had a ten fold increased potassium secretion. After salt restriction and furosemide administration, her potassium secretion rate increased only twofold despite correction of he acidosis. The acidosis, as well as the hyperkalemia, was completely corrected after 9-alpha-Fluorohydrocortisone administration. Hydrochlorothiazide corrected the acidosis and hyperkalemia. Collectively, this picture suggests an underlying chloride shunt as the possible pathophysiological mechanism. Our case in unique in that it is not associated with hypertension.
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PMID:Pseudohypoaldosteronism with normal blood pressure. 886 87

A 15-year clinical follow-up is reported for a familial glomerulopathy characterized on light microscopy by the glomerular deposition of giant fibrillary deposits (Virchows Arch A Pathol Anat Histol 388:313-326, 1980). On electron microscopy, the deposits consist of randomly oriented fibrils (12 to 16 nm in width and 120 to 170 nm in length). These deposits show positive immunoreactivity for fibronectin. One hundred fifty-seven of 197 family members within five generations were investigated. The disease is characterized by the occurrence of albuminuria in the third to fourth decades of life and slow progression to end-stage renal disease over a period of 15 to 20 years with the occurrence of generalized distal tubular acidosis (renal tubular acidosis type IV), hypertension, and the nephrotic syndrome. The frequent occurrence of otherwise unexplained microalbuminuria in young individuals of generations IV and V could be indicative of incipient glomerular disease. In one affected male individual and in his unaffected sister, renal cell carcinoma was diagnosed, raising the possibility that this familial glomerulopathy might be associated with an increased risk to develop renal cell cancer by direct or indirect (associated genetic predisposition) mechanisms. The disease relapsed in one renal transplant, raising the possibility of the presence of a transferable factor that could be part of the deposited fibrillar material or, alternatively, interfere with the glomerular handling of the deposited material.
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PMID:Familial glomerulopathy with giant fibrillar (fibronectin-positive) deposits: 15-year follow-up in a large kindred. 915 3


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