[Urolithiasis as a cause of terminal failure of kidney function and its significance after kidney transplantation].
Explore the source record for details and available documents.
SEARCH · Search PubMed
Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.
Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The functional and morphologic pattern of superficial nephron development was studied in guinea pigs ranging in age between 2 h and 38 days. Concomitent measurements of total kidney function and glomerular counts were also performed. Superficial nephron glomerular filtration rate was found to increase from 0.92 to 19.32 nl/min. The filtration rate of the entire kidney rose from 0.19 to 1.31 ml/min. During the first 15 days of life the average rate of increase in glomerular filtration rate per nephron (0.48 nl/min.day), obtained by dividing the increase in total kidney glomerular filtration rate by glomerular number, was more than twice the observed rate of increase in the superficial nephrons (0.21 nl/min.day). During the remainder of the first month, the increase in superficial nephron glomerular filtration rate (0.97 nl/min.day) was greater than the average increase for all nephrons (0.71 nl/min.day). Thus, the initial increase in total kidney glomerular filtration rate was primarily a consequence of the activity of the deep nephrons, whereas during the ensuing period the superficial nephrons appeared to be the sole contributors to the change in total kidney glomerular filtration rate.The increase in superficial nephron glomerular filtration rate was found to correlate closely with the increase in proximal tubular length. Functional glomerulotubular balance was maintained throughout the entire period of renal maturation.
Since the introduction of percutaneous transluminal renal angioplasty, it has become established as an effective treatment for the correction of renovascular hypertension or the preservation of renal function. However, there has been a general reluctance to use it or other interventional procedures in any patient with a solitary functioning kidney. We attempted renal angioplasty in 11 patients each of whom had a solitary functioning kidney. All 11 had had either a previous contralateral nephrectomy or an autonephrectomy from chronic arterial occlusion. The patients ranged in age from 42 to 81 years. In nine of the 11 patients, a catheter was negotiated across the stenosis, and the lesion was dilated successfully. In two, the lesion could not be crossed. In the group of nine patients whose lesions were dilated successfully, clinical follow-up (2-180 weeks) revealed that hypertension was cured in four and improved in five. Of the two patients in whom angioplasty was not possible, one required emergency renal bypass surgery and the other had no change in renal status. Renal function test results after the procedure were variable and did not correlate with decreases in blood pressure. We conclude that percutaneous renal angioplasty is a satisfactory alternative to surgery for the treatment of renovascular hypertension or the preservation of renal function in a patient with a solitary functioning kidney.
An in vitro perfusion system at 37 degrees C for the assessment of rabbit kidney function is described. The purpose of this assay system is to evaluate the effects of cryobiological manipulation on kidney function. The effect of the colloids dextran (MW = 70,000, 80,000, and 180,000) in the perfusate at 110 mm Hg were compared to a reduced perfusion pressure, colloid-free perfusate. Better function was obtained at lower perfusion pressure with the colloid-free perfusate. Less damage was noted histologically on light and electron microscopy. Investigation of energy substrates on rabbit kidney function demonstrated that butyrate, or lactate, in addition to glucose resulted in increased sodium and glucose reabsorption over glucose alone. Substrate-free perfused kidneys exhibited depressed Na transport. Lactate, and to some extent butyrate, decreased net glucose utilization. An alpha-adrenergic blocking agent, isoxsuprine, in the initial flush solution did not appear to be beneficial. An increase of perfusion pressure from 50 to 75 mm Hg resulted in an increase in GFR. Tubular function was enhanced by inclusion of small amounts of BSA in the perfusate.
A previously published technique for producing renal insufficiency in chicks involves ligating the caudal renal vein together with the ureter near the midpoint of the kidney. This ligation occludes the normal route (caudal renal vein) by which blood exits the medial and posterior kidney divisions. The present study was conducted to evaluate kidney function following chronic caudal renal vein and ureter occlusion. The ureters and caudal renal veins of 2 to 3-week-old chicks were clamped with hemostatic clips (Clamp Group), and kidney function evaluations were conducted when the birds reached 14 weeks of age. Plasma values [osmolality, Na, K, Ca, inorganic P (Pi)] of control, sham, and clamp groups did not differ significantly. Plasma uric acid concentrations did not differ when the control and clamp groups were compared. Clamping the ureter near the midpoint of the kidney caused a significant reduction in the number of filtering glomeruli per kidney, but due to compensatory hypertrophy the kidney weights of the groups did not differ significantly. Kidney function comparisons (urine flow rates, glomerular filtration rates, renal plasma flow rates, urine pH, fractional excretion of Na, K, Ca, Pi, and uric acid) revealed a significant reduction in Na and K excretion by the clamp group, but other renal function parameters did not differ significantly. These experiments demonstrate that chickens have a remarkable capacity to survive significant reductions in renal mass and to adapt to major disruptions of blood flow patterns.
OBJECTIVE: To assess the frequency and possible risk indicators of severe hypoglycemia in insulin-dependent (type I) diabetic patients with impaired kidney function. RESEARCH DESIGN AND METHODS: Retrospective follow-up examination of case subjects and control subjects with mean follow-up periods of 2.9 and 1.3 yr, respectively. The setting was the diabetes center at the Düsseldorf University hospital. Subjects were consecutive type I diabetic patients. Case subjects consisted of 44 patients with initial serum creatinine levels of greater than or equal to 133 microM and pathological proteinuria. Control subjects consisted of 46 patients with normal serum creatinine levels matched for age, duration of diabetes, and hypertension; 57% of case subjects and 67% of control subjects were being treated with beta-blockers. Incidence of severe hypoglycemia (cases/patient-yr) was assessed through an interviewer-administered questionnaire. RESULTS: At comparable levels of HbA1c (7.9 +/- 1.8 vs. 7.6 +/- 1.1%), case subjects had a fivefold higher incidence of severe hypoglycemic episodes (1.28 vs. 0.25 cases/patient-yr, P less than 0.02) than control subjects. Within the group with impaired kidney function, patients with severe hypoglycemic episodes had lower HbA1c levels (7.4 +/- 1.6 vs. 8.7 +/- 2.0%, P less than 0.03) and a lower body mass index (22.0 +/- 3.4 vs. 24.4 +/- 3.8 kg/m2, P less than 0.04) than those without severe hypoglycemic episodes, whereas serum creatinine levels, body weight-related insulin dosage (U x kg-1 x day-1), prevalence of blindness, autonomic neuropathy, and treatment with beta-blockers were comparable. CONCLUSIONS: Type I diabetic patients with impaired kidney function are at an excessively high risk of severe hypoglycemia. In addition to low HbA1c levels, a low body mass index appears to be a risk indicator for this adverse effect of insulin therapy.
The plasma concentration of pancreatic polypeptide (PP-like immunoreactivity) was measured in different vascular beds in order to determine regional kinetics of endogenous PP in fasting, supine subjects with normal or moderately decreased kidney function. Patients with kidney disease (n = 10) had a significantly higher level of circulating PP than controls (n = 10): median PP = 52 (range 21 to 352) v 20 (6 to 143) pmol/L, respectively (P less than 0.02). Circulating PP was inversely correlated to 51Cr-EDTA plasma clearance (r = -0.57, P less than 0.02, n = 14) and directly correlated to serum creatinine concentration (r = 0.70, P less than 0.01). Hepatic venous PP was significantly higher than systemic PP in both controls and patients with kidney disease (P less than 0.001, n = 15). The values were positively correlated (r = 0.98, P less than 0.001; slope = 1.37 +/- 0.05, P less than 0.001), indicating a progressively increasing rate of PP secretion in subjects with raised circulating PP. No statistically significant difference could be detected between systemic and renal venous PP or across the lung, left adrenal gland, or lower limb. Assuming steady state between secretion and biodegradation, the metabolic clearance rate of the peptide was estimated to be approximately 600 to 800 mL/min in controls and slightly below this value in patients with nephropathy. These results suggest that the raised circulating PP found in patients with decreased kidney function is due to both increased secretion and decreased degradation.(ABSTRACT TRUNCATED AT 250 WORDS)
Four studies were conducted to examine the effect of dietary citrate and calcium and modest reductions in kidney function on aluminum utilization in rats. Ingestion of citrate increased retention of aluminum in bones of rats fed 1 mg Al/g diet and increased apparent absorption of zinc. The increased retention of aluminum was not linearly related to dietary citrate levels. These data suggest that citrate had a general effect on the solubility of trace elements in the gut that promoted absorption. When dietary calcium intake was increased from 67 to 250 mumol/g diet, aluminum concentrations in bone were reduced without a change in growth of rats. A reduction (approximately 30%) in kidney function, which was insufficient to alter growth, increased aluminum retention in bone by 34% in rats injected with aluminum and by 13% in rats fed aluminum. Rats fed aluminum seemed to retain in tissues only 0.01 to 0.05% as much aluminum as those injected with aluminum. Thus, tissue concentrations of aluminum, and presumably toxicity, can be altered by moderate changes in diet and kidney function even though overall retention of orally administered aluminum is extremely low.
Influences of treatment with thyroid hormones or dexamethasone during pregnancy on development of kidney function were studied in newborn rats. Treatment of dams for 3 days is followed by a higher rate of urine production in newborn rats. A statistically significant raise of sodium/potassium ratio in tetraiodothyronine- or dexamethasone-treated rats indicates a higher degree of maturation of kidney function. Treatment of dams with dexamethasone is followed by an increase of absolute excreted quantities of sodium and potassium in newborn rats. Treatment of dams with triiodothyronine can increase renal excretion of p-aminohippurate in newborn rats.
Explore the source record for details and available documents.
Hypertension is often seen in Type 1 and Type 2 diabetic patients, particularly in those with nephropathy, and the progression of diabetic nephropathy is closely related to blood pressure elevation. Thus, the effects of antihypertensive drugs on kidney function and insulin sensitivity in diabetic patients are of great clinical importance. Successful antihypertensive treatment has been shown to slow the progression of diabetic nephropathy. Several results from short term studies have suggested that angiotensin converting enzyme (ACE) inhibitors may be advantageous over other conventional antihypertensive agents in reducing albuminuria in both hypertensive and normotensive diabetics with microalbuminuria or persistent proteinuria. However, the decline in glomerular filtration rate during ACE inhibitor treatment is comparable to that during effective treatment with conventional antihypertensive drugs in hypertensive Type 1 diabetic patients with overt nephropathy. Whether ACE inhibitors possess a specific effect in preventing the development of diabetic nephropathy remains to be seen in properly designed long term studies. Although calcium antagonists may preserve kidney function or possess a renoprotective effect in hypertensive Type 2 diabetics with nephropathy, firm evidence supporting this contention seems to be lacking and also requires long term evaluation. Increasing attention is being directed toward the effect of antihypertensive drugs on insulin sensitivity in diabetic patients: ACE inhibitors and alpha 1-adrenoceptor blocking agents have been shown to improve this sensitivity. Despite the widespread involvement of calcium in hormone secretion and action, calcium antagonists appear to have little effects on the glucoregulatory and calcium-regulatory hormones within the drug dosages used in clinical practice. Several clinical variables, such as the presence or absence of hypertension, overt nephropathy and microalbuminuria, or a combination of variables should be accounted for when evaluating critically the cumulative data on the effects of antihypertensive drugs on kidney function and albuminuria in the variety of diabetic patient groups. Understanding the pharmacokinetic and pharmacodynamic characteristics of antihypertensive drugs will be of clinical importance in diabetic patients with advanced nephropathy (glomerular filtration rate of less than 30 ml/min) and/or other complications, such as impaired gastric motility or gastroparesis, and will thereby lead to a more rational management of hypertension in those patients.
The present study aimed at exploring the effect of antihistamine chloropheniramine maleate (H1-blocker) on liver and kidney functions as well as on blood count. 60 mature guinea pigs were used. Histamine or chloropheniramine maleate was given, either alone or together, intramuscularly for 7 successive days. At the end of the experimental period, blood samples were collected for determination of blood counts and of the levels of urea, creatinine, GOT, GPT, and alkaline phosphatase in the sera of different groups. The results showed significant groupwise variations in blood count, liver function as well as kidney function.
The object of this article is to discuss difficulties in extrapolating the performances of a drug for which the kinetic parameters are derived in healthy volunteers, to patients with severely impaired kidney function. The theoretical background of some actual or probable background is given, and a possible solution for these problems is offered, that is, choosing another drug from the same drug group. In patients without kidney function, metabolism is the only pathway of elimination. When the elimination of the metabolite formed occurs by means of renal excretion only, this metabolite accumulates in patients with impaired or absent kidney function. When a metabolic pathway of the parent drug is part of a metabolic equilibrium, the metabolic return reaction results in an "apparent parent compound," with a half-life identical to that of the accumulated metabolite. In this way, the concentration of the "apparent" parent compound increases and the half-life of the sum of parent and "apparent" parent drug will change. Examples of this drug behavior are given for sulfamethoxazole, sulfametrole, sulfamethizole, procainamide, and N4-acetylprocainamide.
Glycaemic control on pump versus pen treatment was evaluated and the effects of optimised metabolic control on kidney function was studied in very long-term uncomplicated insulin-dependent diabetes mellitus (IDDM). Ten otherwise healthy patients participated, age: 36.5 yr +/- 7.9, diabetes duration: 23.7 yr +/- 2.9, urinary albumin excretion (UAE): 5.8 micrograms/min x/ divided by 2.2, se-creatinine and blood pressure were normal and only background retinopathy was present. A 2 x 6 months randomised cross-over study was performed using continuous subcutaneous insulin infusion (CSII) and multiple injection technique (MIT). Glycaemic control was evaluated by a six point profile every two weeks and by measuring HbA1c monthly. At 0, 6 and 12 months, glomerular filtration rate (GFR) and renal plasma flow (RPF) were measured by the constant infusion technique, and UAE by radioimmunoassay. Glycaemic control was significantly better on CSII as compared to MIT (p = 0.01) or pre-study conventional treatment (CT), p = 0.03, whereas there was no difference between MIT and CT. There was no change in kidney function during either treatment. Thus, in these very long-term uncomplicated patients, glycaemic control was significantly improved during CSII. In spite of this, no change was found in GFR, which might suggest that in long-standing diabetes, kidney function is unaltered by changes in metabolic control.
In a clinical study we tested the use of the lysosomal enzyme NAG as a parameter of kidney function. Following prospective randomization, we examined NAG excretion during cisplatin treatment with/without nephroprotection, after intravenous urography with ionic/non-ionic contrast media, during lower/upper urinary tract infections and before/after extracorporeal shockwave lithotripsy for intrarenal calculi (first-generation equipment used). Measurements were performed in 3-h urine specimens and in urine collected over 24 h, using a simple method of analysis. A correlation between NAG leakage and functional disorder of the renal tubular cells seemed likely on the basis of additional clinical and experimental data. Increases, in some cases dramatic, in NAG excretion were observed after the administration of cisplatin and ionic contrast media, in acute pyelonephritis, and after extracorporeal shockwave lithotripsy. However, the increase in NAG excretion was less impressive during cisplatin therapy when nephroprotective amino acids were infused, and in the urography group when non-ionic contrast media were used. Infections of the lower urinary tract did not increase NAG excretion. The results indicate that NAG is a sensitive marker of occult renal dysfunction, which can be checked by non-invasive techniques and can be used in a clinic setting to detect functional disorders of the kidney.
Explore the source record for details and available documents.
The effects of nitrendipine (10 mg b.i.d.) on blood pressure, renin-angiotensin-aldosterone system, and kidney function (by means of glomerular and tubular function) were studied in comparison to captopril (50 mg b.i.d.) and to nitrendipine (10 mg q.d.) + captopril (25 mg b.i.d.) in 30 untreated essential mild-to-moderate hypertensives. The blood pressure lowering effect was similar with either regimen. Nitrendipine showed an acute and chronic natriuretic effect not accompanied by modifications of kidney function. All regimens were well tolerated by the patients without any appreciable side effects over the 4-week study period.