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Indications for and timing of removal of non-functioning kidney transplant.

The clinical indications for and the timing of removal of non-functioning cadaver kidney transplants were studied in 49 of 58 kidneys which had never functioned or which ceased to function in the period 1979-1982. The reason for graftectomy was rejection in 32 cases, rejection and graft infection in eight, surgical complications in eight cases and infection in one case. Nine of the 58 failed kidney grafts were not removed. Graftectomy was performed within a week after diagnosis of graft failure in 24 of the 49 cases. The clinical indications for graftectomy were compared with the morphologic observations in the grafts. Discrepancy was greatest in regard to diagnosis of rejection and primary renal artery thrombosis. Severe complications related to graft failure aggravated the condition in 17 patients and resulted in eight deaths. Based on the findings, a management schedule is proposed. It facilitates postponement or avoidance of graftectomy and minimizes the risk of complications relating to failure of graft function.

Graft Rejection↗

Effect of essential hypertension on kidney function as measured in rat by dynamic MRI.

In this study, dynamic MRI was applied to investigate the effect of genetic hypertension on the renal clearance of Gd(DTPA). Assuming that the paramagnetic agent was essentially cleared through the kidney by glomerular filtration, a first-order kinetic model was used to estimate a rate constant k(cl) describing the transport from the renal cortex to the inner medulla. Experiments were carried out on 12-15-week-old spontaneously hypertensive rats (young-SHR) and age-matched Wistar-Kyoto rats (young-WKY). An additional group of 22-25-week-old SHR (old-SHR) was investigated to assess the long-term effect of chronic hypertension on kidney function. The glomerular filtration rate as measured by the inulin method correlated well with k(cl) results as measured by MRI. A clearance index 30% lower than young-WKY was observed in young-SHR, reflective of a kidney dysfunction. In old-SHR, k(cl) was only 50% of the young-WKY value. As computed from Gd(DTPA) concentration profiles, this translated into delayed time-to-peak (TTP) values, decreased peak Gd(DTPA) concentrations ([Gd](peak)), and a slow elimination of Gd(DTPA) from the blood pool, renal cortex, and inner medulla (e.g., high t(1/2) values). Finally, using the same MRI approach, the data showed that the acute administration of the calcium antagonist verapamil at an antihypertensive dose was followed by a near normalization of SHR renal function. These results indicate that chronic hypertension remains a major pathogenic factor in the progression of glomerular degeneration, as opposed to a primary glomerular defect independent of systemic pressure.

Animals↗

Evaluation of kidney functions and cyclosporine levels in renal transplant patients on Panimum Bioral in post transplant period.

A retrospective analysis of the patients being given Panimun Bioral (microemulsion cyclosporine) after renal transplantation was done at IKRDC, (Institute of Kidney Diseases & Research Centre), Ahmedabad. A total of 21 patients were included for analysis. Patients were evaluated for various parameters e.g. weight, cyclosporine levels, S. Creatinine and BUN at three time schedules as 0 to > or = 30 days, > 30 to > or = 60 days and > 60 to 120 days after renal transplantation. The analysis of data obtained indicates the kidney function tests improved in these patients and therapeutically safe blood cyclosporine levels were achieved in all the three timeschedules.

Cyclosporine↗

Protection of kidney function and decrease in albuminuria by captopril in insulin dependent diabetics with nephropathy.

STUDY OBJECTIVE: To assess whether long term inhibition of angiotensin converting enzyme with captopril and frusemide or bendrofluazide protects kidney function in diabetic nephropathy. DESIGN: Non-randomised controlled before-after trial of matched hypertensive insulin dependent diabetics with nephropathy treated with captopril and frusemide or bendrofluazide. SETTING: Outpatient diabetic clinic in tertiary referral centre. PATIENTS: Treatment group of 18 hypertensive insulin dependent diabetics with nephropathy (mean age 33), who had not been treated previously. Control group of 13 patients (mean age 32) fulfilling the same entry criteria from a prospective study. INTERVENTIONS: Treatment group was given daily captopril 37.5-100.0 mg and frusemide (mean) 98 mg (10 patients) or bendrofluazide (mean) 4 mg (seven). Treatment was continued for about two and a half years. Controls were not treated. END POINT: Measurement of arterial blood pressure, albuminuria, and glomerular filtration. MEASUREMENTS AND MAIN RESULTS: Baseline values were identical in treated and untreated groups respectively: mean blood pressure 146/93 (SE 3/1) mm Hg v 137/95 (2/1) mm Hg; geometric mean albuminuria 982 (antilog SE 1.2) micrograms/min v 936 (1.2) micrograms/min; and mean glomerular filtration rate 98 (SE 5) ml/min/1.73 m2 v 96 (6) ml/min/1.73 m2. Mean arterial blood pressure fell by 8.7 (1.3) mm Hg with captopril and rose by 6.6 (1.5) mm Hg in controls, (p less than 0.001); Albumin excretion decreased to 390 (1.1) micrograms/min with captopril and rose to 1367 (1.3) micrograms/min in controls (p less than 0.001). The rate of decrease in glomerular filtration rate was lower with captopril (5.8 (0.7) ml/year v 10.0 (1.3) ml/year) (p less than 0.01). Rate of fall in glomerular filtration rate and mean arterial blood pressure were significantly correlated (n = 31, r = 0.37, p less than 0.05). CONCLUSIONS: Captopril is a valuable new drug for treating hypertension in insulin dependent diabetics with nephropathy.

Adult↗

Rat kidney function related to tissue glutathione levels.

Rat renal function was evaluated during acute depletion of glutathione (GSH) produced by different doses of diethyl-maleate (DEM). Significant alterations in renal function were observed when the GSH level diminished. The replenishment of GSH and the restoration of renal function were also investigated at various times after the injection. Similar time courses were observed of both the GSH level and renal functions, but the former was shortest. This suggests that the restoration to normal of GSH renal content was necessary in order to regain appropriate kidney function. Furthermore, the fact that impairment of sodium excretion occurred simultaneously with GSH depletion may be considered as evidence of the first event in GSH protective action. It may be hypothetized that the thick ascending limb is the principal renal target for this deficiency.

Animals↗

Kidney function during arterial chemoreceptor stimulation. II. Suppression of plasma aldosterone concentration due to hypoxic-hypercapnic perfusion of the carotid bodies in anaesthetized cats.

The reactions of the mean systemic arterial blood pressure, kidney function (clearance technique) and plasma aldosterone concentration (radio-immuno-assay) elicited by perfusion of the vascularly isolated carotid bodies with venous blood were studied in two series of chloralosed, vagotomized, relaxed, and constantly ventilated cats undergoing saline diuresis. In one group of animals the carotid body chemoreceptors were left intact; in the other one, they were abolished by injecting acetic acid into the glomera carotici. In the cats with intact chemoreceptors perfusion of the carotid bodies with venous blood immediately caused a small and transient increase of the blood pressure, whereas renal plasma flow tended to fall despite continuous chemoreceptor stimulation. Renal fractional sodium excretion already increased in the first 25 min of chemoreceptor stimulation, whereas plasma aldosterone concentration showed a significant decrease only after 45 min of venous perfusion of the glomera carotici. Plasma electrolytes changed only little at that time. No clear relationships between the responses of plasma aldosterone and those of the other parameters measured could be obtained. On subsequent perfusion of the carotid bodies with arterial blood plasma aldosterone returned to the values determined before chemoreceptor stimulation. Inactivation of the carotid body chemoreceptors per se already enhanced plasma aldosterone concentration. Perfusion of the glomera carotici with venous blood in the cats with abolished chemoreceptors did not suppress plasma aldosterone content. The data show that plasma aldosterone changes are not involved in the development of the initial phase (first hour) of the inhibition of renal tubular sodium reabsorption provoked by arterial chemoreceptor stimulation, but during long-lasting chemoreceptor stimulation they might contribute to the maintenance of this type of natriuresis. Furthermore the experiments suggest that the decrease of plasma aldosterone repeatedly observed during exposure of mammals to acute hypoxic hypoxia is possibly the reflex result of the stimulation of the arterial chemoreceptors.

Aldosterone↗

Effect of Etozolin on whole kidney function and fluid and electrolyte reabsorption in rat proximal convoluted tubules and loops of Henle.

The effects of ethyl (Z)-(3-methyl-4-oxo-5-piperidino-thiazolidin-2-ylidene) acetate (etozolin, Elkapin) on whole kidney function and on fluid, sodium and potassium reabsorption in proximal convoluted tubules and loops of Henle of superficial nephrons were studied in rats using clearance and micropuncture techniques. Etozolin (50 mg/kg i.v. initial dose; 50 mg/kg per hour i.v.) markedly increased urinary fluid and sodium excretion and decreased glomerular filtration rate. Fractional tubular sodium reabsorption fell by 8.7%. Fluid and electrolyte reabsorption in the proximal convolution was not significantly influenced by etozolin. The substance significantly increased flow rate, sodium and potassium concentration and decreased tubular fluid/plasma inulin ratio of the early distal tubular, indicating an inhibitory effect on fluid and electrolyte reabsorption in the loop of Henle. Although etozolin is chemically different its site of diuretic action is the same as that of furosemide and ethacrynic acid.

Animals↗