Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0035078 (renal failure)
 31,970 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This study was designed to investigate the effect of tacrolimus (FK506) and of cyclosporine (CsA) on tubular function in renal graft recipients. Patients were randomised after renal transplantation to immunosuppressive treatment with FK506 (n = 8) or CsA (n = 8). Patients had a mean age of 45.7 +/- 3.4 yr; there was no difference in age, sex, HLA status or CMV mismatches. Neither was there any difference in the frequency of episodes of acute kidney failure between the groups, nor was there a significant difference in the frequency of episodes of kidney rejection within the first year. The mean FK506 level at the time lay at 14.7 +/- 14.4 ng/mL whole blood, and the mean CsA level at the time of study was 162 +/- 25 ng/mL whole blood. We performed renal function studies 6 months after transplantation: CIn, CPAH, NaHCO3 loading, and Na2SO4 loading. There was no significant impairment of GFR in patients treated with FK506 with 53.6 +/- 2.5 mL/min as compared to 58 +/- 6 mL in group 2. Plasma renin activity (0.6 +/- 0.4 ng/mL vs 2.3 +/- 3; p < 0.01) and aldosterone (69 +/- 17 vs 157 +/- 28.2 pg/mL; p < 0.05) were significantly decreased during treatment with FK506. Fractional HCO3 excretion was low in both groups, indicating that bicarbonate reabsorption in the proximal nephron was unimpaired. Distal renal tubular acidosis was demonstrated in 4 patients of group 1 but in only 1 of group 2. Potassium levels were slightly increased in patients treated with FK506 (5.4 +/- 0.2 mmoL/L) as compared to cyclosporine (4.9 +/- 0.3 mmoL/L; p < 0.05). Distal hydrogen ion secretion, evaluated by the ability to increase urinary pCO2 in a highly alkaline urine, was impaired in patients treated with FK506 (U-B pCO2: 16.1 +/- 4 vs 36 +/- 5.8; p < 0.05) as compared to patients treated with CsA. The maximum acidification capability (NAE) was slightly lowered during therapy with FK506 (67.5 +/- 11.8 versus 86.6 +/- 16.5 mumoL/min, ns). We conclude that FK506 administration results in a decrease in the rate of hydrogen ion secretion by the collecting tubules. This defect was disclosed by the finding of a subnormal pCO2 in a highly alkaline urine. These results show that FK506 is able to induce distal tubular acidosis. Distal tubular acidosis is part of FK506 induced nephrotoxicity, the pathogenesis of this type of hyperkalemic metabolic acidosis found in patients treated with FK506 after renal transplantation has to be further elucidated.
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PMID:Distal tubular acidosis induced by FK506. 978 58

One year of a very low protein diet (VLPD) can reverse secondary hyperparathyroidism in uremic patients. We studied bone histology, bone mineral density (BMD), and dynamic parathyroid function (calcium/PTH curves) in 16 nondialyzed patients with advanced renal failure who had been receiving a VLPD for a mean of 5 yr (mean protein intake, 0.34 +/- 0.12 mg/kg x day; mean phosphorus intake, 8.2 +/- 2.1 mg/kg x day) and daily supplementation with essential amino acids and their ketoanalogs (1000 IU vitamin D2 and 1-2 g calcium carbonate). Three patients exhibited a high bone formation rate (BFR), 7 patients had normal bone remodeling, and 6 patients had a low BFR, including 2 with osteomalacia and 4 with adynamic bone disease without aluminum overload. A longer diet duration and lower caloric intake were associated with low BFR. More than half of the patients exhibited moderate or severe osteoporosis at the appendicular skeleton. The t score of femur BMD explained 65% of the BFR variance. Patients with a low BFR had a dynamic parathyroid function similar to that of patients with a normal BFR, except they had a lower capacity to buffer a calcium load, whereas patients with a high BFR had a higher basal PTH/maximum PTH and a steeper calcium/PTH curve slope; the calcium set-point was identical in the three groups.
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PMID:Bone mass and dynamic parathyroid function according to bone histology in nondialyzed uremic patients after long-term protein and phosphorus restriction. 1002 9

Twelve patients with renal failure and type A lactic acidosis were treated with haemofiltration during a 30-month period. The first three patients received only lactate-buffered replacement fluid and rapidly succumbed despite the infusion of large quantities of sodium bicarbonate. Bicarbonate-buffered replacement fluid was used for the remaining nine patients, of whom three survived. Haemofiltration with bicarbonate-buffered replacement fluid is an effective method of replacing renal function for this group of critically-ill patients.
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PMID:Treatment of combined renal failure and lactic acidosis by haemofiltration. 1014 41

We previously demonstrated that the large intestine compensated for decreased calcium (Ca) absorption caused by renal failure in rats fed a highly fermentable dietary fiber. In this study, we examined whether the large intestine compensated for insufficient Ca absorption in the rat small intestine without ingestion of a fermentable dietary fiber. Rats were fed one of four test diets containing either insoluble (carbonate) or soluble (gluconate, lactate, or citrate) Ca sources. The dietary Ca level was 2.0 g/kg, which is lower than the minimum requirement for rats (3.0 g/kg), to conduct the present study under a condition in which rats can maximally absorb Ca. To prevent Ca absorption in the small intestine, we replaced a primary phosphate (KH2PO4) with secondary phosphates (K2HPO4 and Na2HPO4) in diets. The apparent Ca absorption in the small intestine was estimated by adding chromic oxide (Cr2O3) as an insoluble and an unabsorbed marker to test diets and by measuring the ratio of Ca:Cr in the cecal content. The apparent Ca absorption in the whole intestine was estimated by the intake and fecal excretion of Ca. The apparent Ca absorption in the small intestine was significantly lower from the Ca carbonate diet than from the Ca gluconate, lactate, or citrate diets. The apparent Ca absorption in the whole intestine was not significantly different among the four groups, and the values were similar to the absorption rates in the small intestines of rats fed diets containing soluble Ca sources. These results show the following: (a) In rats fed 0.2% Ca diets containing soluble Ca salts, Ca is mostly absorbed in the small intestine, even in secondary phosphate intakes; (b) In contrast, in rats fed a 0.2% Ca diet containing an insoluble Ca salt (carbonate), Ca is not sufficiently absorbed in the small intestine. However, the large intestine compensates for the small intestinal Ca absorption decreased by dietary secondary phosphates.
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PMID:The large intestine compensates for insufficient calcium absorption in the small intestine in rats. 1019 5

In patients with chronic renal insufficiency, phosphate retention is a major factor in the development of secondary hyperparathyroidism, renal osteodystrophy, and soft tissue calcification, and may contribute to progression of renal failure. Prevention of phosphate retention with dietary and pharmacological means, along with the administration of calcitriol, may prevent or reverse secondary hyperparathyroidism. With more-advanced renal failure, phosphate binders become necessary to maintain phosphate balance and to prevent hyperphosphatemia. Because of toxicity, aluminum-containing phosphate binders are no longer used. Currently, calcium-containing phosphate binders, such as calcium carbonate and calcium acetate, are the most widely prescribed. Although calcium salts eliminate the problems associated with aluminum toxicity, they often result in transient hypercalcemia, requiring discontinuation of calcitriol and the use of low-calcium dialysate. Several new non- aluminum- and non-calcium-containing phosphate binders are currently at various stages of development, and may provide an alternative to the currently used binders. It is unlikely, however, that the newer compounds will completely replace calcium salts, since mild hypercalcemia may be necessary in chronic renal failure patients to suppress parathyroid hormone production. Other areas of investigation must include the development of drugs to inhibit soft tissue and renal calcifications, and to enhance urinary phosphate excretion.
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PMID:Phosphate binders for control of phosphate retention in chronic renal failure. 1050 31

Sudden cardiopulmonary arrest due to a defective respiratory reflex is observed in diabetic patients. Impaired ventilatory response in diabetic patients to acute hypoxia or hypercapnia induced by the inhalation of an artificial gas has been reported. Little is known regarding the respiratory compensatory ability for mild to moderate metabolic acidosis due to renal failure in insulin-dependent diabetic subjects. Arterial blood pH, HCO3-, PaCO2 and PaO2 were measured in 13 insulin-dependent diabetic subjects with advanced nephropathy and in 33 non-diabetic subjects with end-stage renal failure. The diabetic group consisted of six predialysis patients and seven on regular hemodialysis (HD) and the non-diabetic group, ten predialysis patients and 23 on HD. Differences between measured partial arterial pressure of carbon dioxide (PaCO2) and predicted PaCO2 determined from HCO3- were examined. PaCO2 was significantly higher in the diabetic than in non-diabetic group (40.0 +/- 7.4 versus 31.1 +/- 5.1 mmHg, p < 0.05 in predialysis, 42.0 +/- 6.4 versus 36.0 +/- 2.6 mmHg, p < 0.05 in HD), though plasma pH was essentially the same for either. Differences in measured PaCO2 and predicted PaCO2 were significantly larger in the diabetic group than in non-diabetic group. Ventilatory response to uremic acidosis may thus be considered impaired in subjects with advanced diabetic nephropathy.
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PMID:Impairment of ventilatory response to metabolic acidosis in insulin-dependent diabetic patients with advanced nephropathy. 1051 94

Uremic patients on maintenance hemodialysis are in positive phosphate balance. This is mainly the result of the complex elimination kinetics of phosphate during dialysis. Removal of phosphate is less than net dietary intake. Classical phosphate binders such as calcium carbonate, calcium acetate, and aluminum-based compounds are limited by side effects (hypercalcemia) and outright toxicity (aluminium). There have been numerous recent attempts to develop alternative phosphate binders, e.g., polyallylamine-hydrochloride (Renagel), lanthanum carbonate, and trivalent iron-containing compounds. The latter is based on old observations that iron salts may cause hyperphosphatemia and rickets in experimental animals and in patients. This idea has recently been taken up again, and effective inhibition of net intestinal phosphate uptake in non-uremic and uremic rats has been shown using simple iron salts (citrate, chloride, ammonium citrate) and complex compounds (cross-linked dextran and stabilized polynuclear iron hydroxide). In uremic rats, the latter compound reduces urinary phosphate excretion as an indicator of reduced intestinal phosphate uptake and has also been shown to be effective in subjects with preterminal renal failure. So far, no side effects or short-term toxicity has been observed. The compound appears promising and deserves further evaluation.
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PMID:Phosphate binders on iron basis: a new perspective? 1063 63

The serum anion gap (AG) is a calculated value defined as the difference between the sum of sodium and potassium and the sum of chloride and bicarbonate concentrations. Thus, the anion gap is equal to the unmeasured cations minus the unmeasured anions (UA). To evaluate the AG changes during HDF-on line, we studied 20 patients treated with this technique. Blood pH, HCO3, NA, K, Cl, albumin, phosphorus, urea, creatinine and lactate were determined pre and post-HDF. The AG, negative charger of serum albumin (CAA) and phosphate (CAP) were computed by equations. AG decreased during HDF from 23.1 +/- 3.4 mEq/l to 17.3 +/- 3.6 mEq/l (p < 0.001). The CAA rose from 10.9 +/- 0.8 to 12.3 +/- 1.7 mEq/l (p < 0.001). The CAP and lactate fell significantly during HDF (p < 0.001 and 0.05 respectively). Other unmeasured anions (UA) decreased from 7.9 +/- 3.0 to 2.4 +/- 2.7 mEq/l (p < 0.001). The CAA contributed 47.7 +/- 6.5% and 73.01 +/- 12.7% to the pre and post-HDF serum anion gap respectively. The CAP accounted for 12.4 +/- 3.4% and 8.6 +/- 1.8%, lactate 6.4 +/- 3.9% and 6.0 +/- 3.0% and UA for 33.2 +/- 7.7% and 12.2 +/- 13.6% of the anion gap pre and post-HD respectively. AG and UA correlated significantly with blood urea pre-HDF and urea generation. The increase in serum albumin and pH can mask an decreased concentration of unmeasured anions in patients treated with HDF on-line. An adjusted anion gap without effect of CAA and CAP can be obtained. With the help of this adjustments the changes in some undetermined anions organic and inorganic (sulphate and others in renal failure) can be calculated.
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PMID:[Changes in the anion gap in patients undergoing hemodiafiltration]. 1082 25

Chronic renal failure patients on maintenance hemodialysis (HD) have a number of ECG abnormalities and cardiac arrhythmias. Clinical and experimental data have shown that increased QT dispersion is associated with severe ventricular arrhythmias and sudden cardiac death. Therefore, the aim of this study was to investigate whether the uremic patients receiving long-term HD have increased QTc interval and/or QTc dispersion compared to normal subjects and to evaluate the effect of electrolyte changes between the predialysis and postdialysis phases on these parameters. Forty patients with end-stage renal failure on long-term HD (22 men, 18 women, mean age 44 years) were included in this study. Serum concentrations of K+, Na+, Ca++, Mg++, Cl-, phosphate, urea, creatinine, HCO3-, and arterial blood gases (PO2, PCO2), together with blood pH, were monitored and QTc intervals and QTc dispersion were measured from 12-lead ECG in predialysis and postdialysis phases. The hemodialyzed patients had an increased predialysis QTc maximum interval and QTc dispersion compared to normal subjects (480 +/- 51 vs 310 +/- 38 msec, p < 0.001 and 61 +/- 17 vs 42 +/- 14 msec, p < 0.001, respectively). Both QTc maximum interval and QTc dispersion increased significantly at the end of the HD (480 +/- 51 vs 505 +/- 49 msec p < 0.001 and 61 +/- 17 vs 86 +/- 18 msec, p < 0.001, respectively). The serum K+ (5.3 +/- 0.56 vs 3.36 +/- 0.41 mEq/L, p < 0.001), phosphate (7.19 +/- 1.62 vs 3.81 +/- 1.02 mg/dL, p < 0.001), magnesium (0.87 +/- 18 vs 0.75 +/- 0.14 mg/dL) and urea concentrations (174 +/- 22 vs 74 +/- 14 mg/dL, p < 0.001) significantly decreased, whereas the Ca++ (2.21 +/- 0.18 vs 2.47 +/- 0.24 mg/dL, p < 0.001), HCO3- (15.5 +/- 3.2 vs 20.1 +/- 3.4 mmol/L, p<0.001) concentrations and pH (7.27 +/- 1.1 vs 7.43 +/- 1.2, p < 0.001) significantly increased after HD compared to predialysis values. There was significant correlation between the QT dispersion increase and serum electrolyte changes (K+, Ca++, and pH levels) (p < 0.05). The association between serum electrolyte changes, acid-base status and QT measurements might provide new insights into the evaluation of the ionic bases involved in inhomogeneous ventricular repolarization.
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PMID:Increased QT interval dispersion after hemodialysis: role of peridialytic electrolyte gradients. 1087 Aug 59

To investigate the effect of biofiltration (BF) on the ability of blood to supply oxygen to the peripheral tissues, a 2 week crossover study was conducted with bicarbonate hemodialysis (BcHD) and BF using 5 male patients with diabetic renal failure as subjects. BcHD and BF were performed for 4 h and 3.5 h per session, respectively. Blood gases, the pH of red blood cells (RBC-pH), and 2. 3-diphosphoglycerate in RBC (RBC-2.3DPG) were measured during each treatment. After a 2 week BF treatment, the plasma HCO3- at the beginning of BF was significantly higher than that of BcHD (p < 0.01), and the blood pH improved with an elevated plasma bicarbonate level (p < 0.05). The RBC-pH at the beginning of BF was higher than that of BcHD (p < 0.05) although the RBC-pH at the end of both therapies increased to similar levels. The RBC-2.3DPG during BcHD remained unchanged, but during BF significantly increased (p < 0.05). Metabolic acidosis was significantly improved by BF with its effect reaching to the RBC intracellular level. The improved metabolic acidosis might occur as a result of the increase in RBC-2.3DPG during BF. This increase in RBC-2.3DPG has the effect of reducing the affinity of oxygen for hemoglobin and allows more oxygen to be delivered to the peripheral tissues although the increase in RBC-pH by dialysis restricts the dissociation of oxygen from hemoglobin.
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PMID:The effect of biofiltration on red blood cells 2.3-diphosphoglycerate and pH. 1112 79


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