Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fawn-hooded (FH) rats develop low-renin hypertension which is preceded by a decrease in urinary kallikrein. We examined urinary excretion of active and inactive kallikrein in hypertensive FH male rats and matched animals of the ancestral, normotensive Wistar strain. To determine the effects of modulation of salt intake on the kallikrein profile, rats were given standard rat chow (0.39% NaCl), a low-salt diet (0.02% NaCl), or a high-salt diet (standard chow plus water with 1% NaCl). Control FH rats excreted less active kallikrein (p less than 0.02), had similar amounts of inactive kallikrein, and had a higher inactive/active kallikrein ratio (p less than 0.02) than control Wistar rats. Low salt intake increased active kallikrein 136% (p less than 0.002) and 54% (p less than 0.035) in FH and Wistar rats, respectively, but did not change the level of inactive kallikrein or the inactive/active kallikrein ratio. High salt intake had no effect on kallikrein excretion in either strain. Low salt intake did not change blood pressure in either strain in spite of significant changes in plasma renin activity, angiotensin II and active kallikrein excretion. The low urinary active kallikrein and the high inactive/active kallikrein ratio in FH rats do not appear to play a role in the established hypertension in the FH rat, since modulation of these parameters did not cause a significant change in the elevated blood pressure.
Nephron 1989
PMID:Modulation of urinary kallikrein and plasma renin activities does not affect established hypertension in the fawn-hooded rat. 264 67

Triamterene (TA) is a mild 'potassium-sparing' diuretic usually employed in combination with other more potent diuretics in the treatment of hypertension. TA pharmacokinetics and pharmacodynamics in normal volunteers, elderly subjects and in patients with renal and hepatic dysfunction are reviewed. A variety of adverse renal effects, such as abnormalities in urinary sediment, nephrolithiasis, interstitial nephritis and acute renal failure, has been reported to occur and is also reviewed. Of particular concern with the increased availability of 'over-the-counter' nonsteroidal anti-inflammatory medications (NSAID) is the adverse interaction between TA and NSAID which may culminate in acute renal failure. Although a rare occurrence, the clinician should be aware of potential adverse reactions associated with the use of TA.
Nephron 1989
PMID:Triamterene and the kidney. 266 34

This study was undertaken to evaluate the relation between the urinary excretion of guanidinoacetic acid (GAA) and other substances in hypertensive patients (6 with borderline hypertension and 29 with hypertension) and 12 normal controls. In 10 of the hypertensive patients, GAA was measured before and after 4 weeks of treatment with calcium entry blocker. In hypertensive patients the rate of GAA urinary excretion was 43.5 +/- 17-4 micrograms/min, which was much lower than in the controls (77.2 +/- 35.9 micrograms/min) (p less than 0.01). There was no significant difference among these groups in creatinine clearance (CCr), serum creatinine (Cr), beta 2-microglobulin (BMG) or in the urinary excretion of BMG, N-acetyl-D-glucosaminidase (NAG) or radiosensitive microalbumin (mAlb). The urinary excretion rate of GAA was positively correlated with CCr (r = 0.62; p less than 0.01), and negatively correlated with mean blood pressure (r = -0.49; p less than 0.01). Finally, the GAA excretion was significantly correlated with urinary NAG (r = 0.24; p less than 0.05) and serum BMG (r = -0.31; p less than 0.05), but not with urinary mAlb (r = 0.12; p less than 0.05). Ten hypertensive patients followed for 4 weeks attained their ultimate mean blood pressure reduction after treatment (from 119.3 +/- 8.0 to 101.7 +/- 13.5 mm Hg; p less than 0.001), but the GAA/Cr ratio in the urinary excretion was significantly elevated (from 0.054 +/- 0.016 to 0.070 +/- 0.02; p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)
Nephron 1989
PMID:Urinary excretion rate of guanidinoacetic acid as a new marker in hypertensive renal damage. 266 50

From 1978 through 1984, the incidence of treated end-stage renal disease (ESRD) secondary to diabetic nephropathy increased from 3 to 19 per million population among the membership of the Kaiser Permanente Medical Care Program in Northern California. Forty-eight percent had type II diabetes. Among 66 type II diabetics retinopathy was less severe and hypertension was more frequent than among 50 type I diabetics. Blacks were represented in a higher proportion than expected from their proportion of the health plan membership. Among type II diabetics who developed ESRD, once proteinuria occurred, nephropathy progressed at the same rate observed in type I diabetics. This observation suggests that the clinical progression of diabetic nephropathy may be similar for both types of diabetes after the development of proteinuria, but requires prospectively collected data for confirmation.
Nephron 1989
PMID:Comparison of type II and type I diabetics treated for end-stage renal disease in a large prepaid health plan population. 273 29

Three cases of pseudohyperaldosteronism produced by the application of an antihemorrhoid cream containing 9 alpha-fluoroprednisolone are reported. All three presented edema, hypokalemia and metabolic alkalosis. Two of the patients also exhibited slight arterial hypertension. This iatrogenic possibility must be ruled out in cases of hypermineralocorticoidism, thus avoiding unnecessary and costly examinations.
Nephron 1989
PMID:Pseudohyperaldosteronism due to application of an antihemorrhoid cream. 273 69

Among 98 patients with IgA nephritis who had protein selectivity studies performed, 54% had nonselective proteinuria and the remaining 46% had selective proteinuria. Patients with nonselective proteinuria had a higher incidence of glomerulosclerosis. At the end of a 4-year follow-up period, patients with nonselective proteinuria had lower creatinine clearance, higher incidence of hypertension and chronic renal failure when compared to patients with selective proteinuria. Six out of eleven patients (55%) in the study who had the nephrotic syndrome had selective proteinuria. Among these 6 patients, 1 had spontaneous remission and 5 responded to steroid or cyclophosphamide therapy. The remaining 5 patients with nonselective proteinuria did not respond to therapy. In the patients who had selectivity studies repeated, the data showed that the selectivity index (SI) can fluctuate depending on the clinical course of the patients. SI can therefore be used to monitor the progress of patients on long-term follow-up. Protein selectivity appears to be a useful prognostic index in IgA nephritis. For patients with the nephrotic syndrome it may serve as a guide to therapy.
Nephron 1989
PMID:Protein selectivity: a prognostic index in IgA nephritis. 277 Sep 44

Renal hemodynamics and sodium excretion were determined before and during infusion of dopamine in doses ranging from 0.25 to 8 micrograms/kg/min in healthy volunteers (n = 15) and in patients with renal disease and moderately impaired renal function (n = 21, baseline glomerular filtration rate 34-85 ml/min). While in normal volunteers dopamine resulted in marked renal vasodilation (maximal fall in filtration fraction 24%), in patients with moderately impaired renal function, the renal vasodilatory response to dopamine was impaired (maximal fall in FF 13%) and was found to depend on baseline glomerular filtration rate. Infusion of dopamine in doses of 2 micrograms/kg/min and higher resulted in an increase in urinary sodium excretion, which was comparable for healthy volunteers and patients with renal disease. We conclude that dopamine results in a predominantly efferent glomerular vasodilation and, therefore, may be salutary in lowering intraglomerular hypertension. However, in patients with renal disease the renal hemodynamic response to dopamine infusion is impaired compared to healthy volunteers, while the natriuretic response is maintained.
Nephron 1989
PMID:Impaired renal hemodynamic but conserved natriuretic response to dopamine in patients with renal disease. 277 Sep 50

A 19-year-old man with renal failure and mild hypertension was found to have juvenile nephronophthisis. The diagnosis was established by computerized tomography of the kidneys after other imaging techniques had proved inconclusive. Computerized tomography is advocated as the investigation of choice if this diagnosis is considered.
Nephron 1989
PMID:Nephronophthisis-cystic renal medulla complex: diagnosis by computerized tomography. 277 4

The factors that influence the progression of renal failure in analgesic-associated nephropathy (AAN) still remain to be clarified. In this study, the actual analgesic intake (N-acetyl-p-aminophenol, NAPAP, i.e. acetaminophen in urine) and progression of renal failure (1/crea method) in 127 outpatients with various renal diseases were investigated over a period of 7-150 months. AAN was diagnosed in 57 of the 127 patients (44%). The NAPAP test was positive in 21% of the 57 AAN patients and in 3% of the 70 control patients with other renal diseases (p = 0.0001). The AAN patients presented with more advanced renal insufficiency, lost more weight, and had more severe hypertension as well as a higher mortality rate than the control patients (univariate analysis). Progression of renal insufficiency, as measured by regression analysis of the reciprocal of serum creatinine versus time and expressed as clearance loss per year, was more rapid in the AAN patients who were found positive for NAPAP (6.9 +/- 5.5 ml/min/year) than in the AAN patients who were found negative (4.1 +/- 11.0 ml/min/year) or in control patients with other renal diseases (5.1 +/- 14.9 ml/min/year). Multivariate analysis showed the more rapid clearance loss to be the most discriminating factor between the AAN patients who continued analgesic abuse of phenacetin-or acetaminophen-containing drugs and AAN patients who stopped. We therefore conclude that continued analgesic abuse promotes renal insufficiency in AAN. The progression of renal failure in AAN patients who stopped abusing analgesics, however, cannot be explained within the parameters investigated, i.e. urinary tract infection, hypertension, hyperalimentation, or papillary necrosis.
Nephron 1989
PMID:Progression of renal failure in analgesic-associated nephropathy. 279 44

We report 3 cases of acquired cystic disease of the kidneys with associated renal carcinoma in 2 of the cases. In all 3 cases, the patients had chronic renal insufficiency due to hypertension but had never required dialysis. Review of 176 reported cases of acquired cystic disease of the kidneys and renal tumors disclosed that 18 patients (including 1 previously reported by us) had never received dialysis treatment. These cases support the hypothesis that acquired cystic disease of the kidney is not restricted to patients treated with maintenance dialysis. Among the 18 patients, hypertension was the most common underlying cause of renal failure. Patients with chronic renal failure due to or associated with severe hypertension should be monitored carefully for the development of both renal cysts and tumors even though they have not started on chronic dialysis.
Nephron 1989
PMID:Acquired cystic disease of the kidneys and renal cell carcinoma in chronic renal insufficiency without dialysis treatment. 281 71


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>