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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The functional renal failure accompanying advanced liver disease is characterized by azotemia, a urine of very low sodium concentration and systemic hypotension with decreased renal perfusion and high renal vascular resistance. Patients with this disorder have a markedly reduced ability to excrete free water and develop hyponatremia, ascites and edema. It is postulated that this renal dysfunction is due to hepatic failure to make renin substrate. Renin released from the kidney is thus unable to exert its pressor effect. The resultant hypotension and renal hypoperfusion continue to stimulate excessive synthesis and release of renin. It is postulated that the overdriven renal renin system increases renovascular resistance at the level of the glomerular arterioles. This causes decreased renal blood flow and decreased glomerular filtration rate leading to salt and water retention and azotemia. Since no renin substrate is available for human infusion, this hypothesis could be tested either by infusion of angiotensin II to restore systemic blood pressure and renal perfusion or by beta adrenergic blockade with propranolol to attempt to decrease the intrarenal effects of renin, restore glomerular blood flow and filtration and thus return of renal function.
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PMID:Hepatorenal syndrome: a disease mediated by the intrarenal action of renin. 77 56

With improving standards of antenatal care, severe pre-eclampsia dn eclampsia are becoming less common and experience in the management of these conditions is lessening. Co-ordinated plans for the care of patients should be established by obstetricians and anaesthetists working as a team. A suitable regime for drug therapy in severe pre-eclampsia or eclampsia is the following: Initial management Diazepam 10 mg slowly i.v. Pethidine 100-150 mg i.m. or i.v. in incremental dosage, or extradural blocks, if analgesia is also required. Hydrallazine 20 mg i.v. initially, followed by 5 mg at intervals of 20 min until the diastolic pressure is less than 110 mm Hg. Then, preferably by syringe pump in a concentration of 2 mg/ml, at a rate of 2-20 mg/h. If vomiting occurs this can be controlled by administration of atropine. Subsequent management Sedation and anticonvulsant therapy. Continue diazepam and, in severe cases, institute chlormethiazole infusion. Continue analgesia with pethidine or extradural block. Control of hypertension by adjusting the dose of hydrallazine. If tachycardia exceeds 120 beat/min give propanolol 2-4 mg i.v. Plasma protein depletion with groww oedema is treated by administration of salt-free albumin or plasma protein fraction. Diuretic therapy is indicated if there is gross oedema or signs suggestive of acute renal failure. Oliguria associated with increased blood urea may be a result of renal failure or dehydration. The latter should be evident from the patient's condition and central venous pressure, but i.v. fluids and frusemide 20-40 mg can be used as a therapeutic test. Mannitol reduces cerebral oedema and may be given if diuresis has been first produced with frusemide. Potassium chloride is given if the plasma potassium decreases to less than 3 mmol/litre. Heparin therapy is considered if there is clinical evidence of disseminated intravascular coagulation.
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PMID:The management of severe pre-eclampsia and eclampsia. 83 44

The effect of propranolol therapy on the mean arterial pressure (MAP) and plasma renin activity (PRA) was studied in three groups of hypertensive patients who were also treated with saliuretics. Group A: In 14 patients with essential hypertension on chlorthalidone treatment, an additional daily dose of 640 mg propranolol for two months led to a significant reduction of the MAP (from 124 to 105 mm Hg) and PRA (from 5.3 to 2.0 ng AI/ml/hr standing). There was no correlation between MAP reduction and either the original levels or change in PRA. Group B: In 14 patients with essential hypertension and 5 with renal artery stenosis studied on a fixed salt intake, the plasma and extracellular volumes, PRA, and blood pressures were recorded before and after three days of diuretic induced salt depletion and, with maintenance of the depleted state, after three days of propranolol. Salt depletion resulted in a decrease in MAP from 132 to 128 mm Hg (NS), and PRA increased from 3.4 to 22.3 ng AI/ml/hr (P less than 0.01). There was no correlation between change in MAP and PRA control values, PRA change, or any of the volume parameters. Addition of propranolol was followed by a rapid MAP decrease to 111 mm Hg (P less than 0.01), and the PRA dropped to a mean of 8.5 (P less than 0.01). No correlation was found between change in MAP and change in PRA. The patients with renal artery stenosis did not differ in their reactions from those with essential hypertension. Group C: In five patients with moderate renal failure and normal to expanded 82-Br distribution volume, propranolol lowered MAP by 10% and lowered the PRA in all five. Salt depletion by furosemide to 82-Br volumes below normal resulted in a 10% decrease of MAP and a marked rise in PRA. In this state propranolol was followed by a further MAP reduction of 18% and a decrease in PRA. There was no quantitative relationship between MAP and PRA change during either of the treatment regimes. It is concluded that in various forms of hypertension, the blood pressure can be effectively lowered by combining diuretics and propranolol regardless of the pretreatment PRA level.
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PMID:Effect of salt depletion and propranolol on blood pressure and plasma renin activity in various forms of hypertension. 109 56

The influence of dietary salt on the levels of plasma bicarbonate and on the characteristics of bicarbonate reabsorption was studied in experimental chronic renal failure. Chronic renal failure was produced in rats by sequential partial nephrectomies. The control group received a diet constant in salt content throughout the progression of renal failure; the other group (PRNa), at each stage of renal failure, received salt intake reduced in direct proportion to the fall in glomerular filtration rate (GFR). In the steady state, the quantities of urinary sodium closely approximated intake in obth groups of animals. The adaptive increased natriuresis per nephron exhibited by the control animals was prevented in the PRNa animals. The PRNa group had (a) higher plasma bicarbonate levels, (b) increased bicarbonate thresholds, and (c) increased maximal tubular reabsorptive capacity for bicarbonate. As renal failure progresses, dietary salt can become a determining factor of the levels at which plasma bicarbonate is maintained. Proportional reduction of dietary salt results in bicarbonate conservation in rats with experimental progressive renal failure.
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PMID:The influence of salt intake on the metabolic acidosis of chronic renal failure;. 115 Aug 71

A 22 year old man with renal failure associated with salt wasting, retinitis pigmentosa, and imino acid abnormalities is reported. Renal tissue showed changes compatible with medullary cystic disease or juvenile nephronophtisis. Special studies were carried out to clarify the mechanism of renal salt wasting. Retinal pigmentary changes were found in three siblings and a male cousin; in two siblings studied abnormal retinal function was demonstrated. the parents who were first cousins once removed were normal. Fifty kindred members were examined and none showed unequivocal signs of renal disease. Autosomal recessive transmission of ocular and renal disease appeared likely. The separation of medullary cystic disease from juvenile nephronophthisis on the basis of onset and mode of inheritance is probably artificial.
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PMID:Cystic disease of the renal medulla associated with retinitis pigmentosa and imino acid abnormalities. 115 47

The case report of a 27-year-old woman who had been normotensive before her 1st pregnancy 6 years earlier is presented. At 2 months postdelivery she began taking estro-progesterone. She was given Enidrel R (norethynodrel 4.925 mg, mestranol .075 mg) for 18 months and then Ovariostat (lynestrenol 2.5 mg, mestranol .075 mg). Her blood pressure was not recorded until 2 years later when it was 180 mm Hg systolic. Contraceptive therapy was then stopped. A month later pregnancy occurred. At that time her blood pressure was 120 mm Hg. The delivery was normal. 4 months later she began taking Ovariostat again. Headaches soon developed and her blood pressure was found to be 270/150 mm Hg. On admission to the hospital 3 weeks later her blood pressure was 250/100 mm Hg. Renal failure was present. Creatinine clearance was 12 ml/minute. No cause for this hypertension was found. 1 month later hypertension was 210/160 mm Ha. Retinal hemorrhaging had lessened but azotemia persisted. Heart failure and oliguria followed. Dialysis was done weekly. A bilateral nephrectomy was done. Microscopic study of renal tissue showed malignant nephroangiosclerosis. After 10 days her blood pressure was 150/100 mm Hg. Her general condition improved. A salt-free diet was prescribed. Blood pressure subsided to 140/80 mm Hg before dialysis. A renal graft was done and 10 months later blood pressure was normal. These hypertensions are usually benign and subside when the contraceptive therapy is discontinued. When estrogen-progesterones are prescribed, blood pressures should be recorded frequently and therapy stopped if hypertension arises.
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PMID:Malignant hypertension with irreversible renal failure due to oral contraceptives. 119 51

The potassium-containing salt substitute sanasol was examined for its effects on blood pressure and renal function in normo- and hypertensive rats, as well as on the edematous syndrome in circulatory insufficiency. The antihypertensive and occasional antiedematous effects of sanasol resulted in unfavorable changes in electrolyte balance. Sanasol was found to be ineffective in experimental renal failure.
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PMID:[The effect of the table salt substitute sanasol on arterial pressure, water-salt metabolism and kidney functions in experimental pathology of circulatory homeostasis]. 130 67

In cirrhotic patients without renal failure, salt retention could result from a decreased effective intravascular volume or could be a primary event leading to increased intravascular volume. Clearance of urea and uric acid depend on an effective intravascular volume. In the syndrome of inappropriate secretion of antidiuretic hormone (SIADH)--a state of increased intravascular volume--uric acid clearance is increased and that of urea is increased only when salt excretion is low. The intravascular volume of 60 consecutive cirrhotic patients without renal failure was estimated indirectly by studying the relationship between fractional excretion of filtered (FE) sodium, urea, and uric acid. Forty five per cent had a high FE uric acid (> 12%), which could mean a high intravascular volume, and presented with an FE urea that was inversely correlated with FE sodium (r = 0, 62; p < 0.001) as in SIADH, while in the controls the FE urea was positively correlated with FE sodium (r = +0, 46; p < 0.01). In patients who had a normal FE uric acid and low FE sodium (< 0.2%), the FE urea was significantly lower (40 (13)%, n = 20) than in subjects with high FE uric acid and a low FE sodium (61 (9)%, n = 16, p < 0.001); this last group also presented with lower mean blood urea concentrations (3.1 (1.2) mmol/l and 4.0 (1.8) mmol/l; p < 0.05) and a lower supine renin activity (p < 0.01). As observed in the SIADH, cirrhotic patient with high FE uric acid have raised FE urea only when salt excretion is low. It is believed that the low salt excretion is not caused by a decrease in effective intravascular volume and that this is increased in cirrhotic patients with raised FE uric acid.
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PMID:Raised urea clearance in cirrhotic patients with high uric acid clearance is related to low salt excretion. 139 36

Farr's assay using double-stranded (ds) DNA from E. coli is a most sensitive and specific method for the detection of anti ds-DNA antibodies in patients with systemic lupus erythematosus (SLE). Because of the lack of sufficient DNA antigens, however, final antibody titers were hardly determined when the sera contained antibodies titered more than 100U/ml (or more than 60 per cent by DNA binding activities). In such sera DNA binding activities were measured by using ds-DNA tracer adjusted final concentration of NaCl to 125 mM. Higher binding activities measured by high-salt tracer are obtained significantly in SLE patients groups with nephrotic syndrome, proteinuria, cast, renal failure, diffuse proliferative nephritis, low serum complement levels, anemia and/or low IgG/IgA levels compared with the patients who lacked these clinical findings. In contrast the patients with digital rash or cramp showed significantly lower high-salt binding activities. The patients with pleuropericarditis tended to have lower bindings. The non-lupus patients including MCTD also had lower levels. These clinical characteristics could not be evaluated by standard Farr's assay. High-salt bindings suggest the presence of high avidity antibodies and also partly may mean the high levels of low avidity antibodies. The application of high-salt binding activities, thus, is a useful tool for the evaluation of clinical characteristics of SLE patients who had high levels of anti ds-DNA antibodies by standard Farr's assay.
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PMID:[Reassessment of measurement of anti double-stranded DNA antibodies by Farr's assay using double-stranded DNA from E. coli and application of DNA binding Activities in high salt solution]. 144 79

Renal failure was found in a five-year-old patient who had been treated with insulin since he was diagnosed as having insulin dependent diabetes mellitus (IDDM) at 3 years of age. Laboratory data showed that his renal failure was caused by a renal tubular dysfunction. The autopsy findings of his pancreas were compatible with those of IDDM. The kidneys were atrophied with an innumerable number of crystals in the proximal tubuli. Staining by Kossa indicated that the crystals contained calcium salt. The calcium content of his kidneys was significantly higher than that of control. The nephrocalcinosis seems to be caused by hypercalciuria associated with IDDM.
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PMID:Insulin dependent diabetes mellitus accompanied by nephrocalcinosis and renal failure. 144 54


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