Chronic renal failure: renal bone disease.
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Unwanted corticosteroid effects in childhood bone marrow failure, renal failure and brain damage: case report.
The case report of the corticosteroid complication in an eight-year-old girl with immune thrombocytopenic purpura is presented. She was treated with high dosage corticosteroids and incurred severe side effects, including bone marrow depression, renal magnesium stones, osteoporosis, depression of affect, convulsions with cerebral damage and adrenal suppression.
Bone Marrow Diseases↗
Normal renocortical blood flow in experimental acute renal failure.
Renal cortical blood flow of rats with postischemic, myohemoglobinuric, and mercury-induced acute renal failure was measured by the hydrogen washout technique using implanted platinum electrodes. Total renal blood flow was determined by venous cannulation in separate series of rats. The values obtained with the two methods were in excellent qualitative agreement (r=0.99, P less than 0.001), although venous cannulation gave values that were constantly lower than those calculated for whole kidney from the cortical flow rate and assumed cortical mass. Myohemoglobinuria produced by glycerol injection caused cortical blood flow to fall from a control value of 7.37+/-0.23 (SEM) ml/min X g of cortex to approximately one-half that value for four hours after injection (P less than 0.001). Flow rates 12 and 24 hr after glycerol injection were 85% (P less than 0.001) and 90% (P less than 0.05) of control, respectively. Cortical flow was reduced to 5.49+/-0.39 (SEM) ml/min X g of cortex four hours after release of one hour's total bilateral renal arterial occlusion (P less than 0.001), but rose to normal within 24 hr. Poisoning with 4.7 mg/kg of body wt of mercuric chloride produced a cortical blood flow value that was 30% higher than control 24 hr after injection (P less than 0.01), while a 12 mg/kg of body wt dose gave a normal flow value. Inulin clearance was severely depressed in all models at all study times. Thus, in contrast to human acute renal failure, marked renal cortical ischemia is not an essential feature of these different forms of murine acute renal failure.
Acute Kidney Injury↗
Natriuresis-induced protection in acute myohemoglobinuric renal failure without renal cortical renin content depletion in the rat.
The interrelationships of renal cortical renin content RCRC, sodium chloride excreting and the severity of renal failure were studied in the glycerol-induced acute myohemoglobinuric renal failure model in the rat. Protocols were designed to increase sodium chloride excretion without necessarily resulting in RCRC depletion. Our data fail to demonstrate a relationship between RCRC and severity of renal failure, but they demonstrate an excellent inverse correlation between the sodium chloride excretion of the animals in the 24 h prior to glycerol administration and the severity of resulitng renal failure. The protection of long-term saline-drinking animals should properly be ascribed to the associated natriuresis which develops much before RCRC depletion during the time course of saline drinking. The exact mechanism by which natriuresis exerts its protective effect needs further elucidation, but our data argue against a major role for RCRC in the pathogenesis of acute experimental renal failure.
Acute Kidney Injury↗
Persistent acute renal failure with renal artery stenosis: cure following reconstructive arterial operation.
A case of acute renal failure is reported in which renal function returned after surgical correction of renal artery stenosis to the sole functioning kidney. Acute renal failure associated with renal vascular lesions is reviewed. Although often clinically apparent vascular obstruction may be asymptomatic and should be considered in cases of prolonged acute renal failure.
Acute Kidney Injury↗
Renal osteodystrophy in end-stage renal failure.
Renal osteodystrophy has many skeletal pathologic features, eg, fibroosteoclasia (osteitis fibrosa), osteomalacia, osteopenia, pseudofracture, cyst formation, and osteosclerosis. Many of these are caused by the secondary hyperparathyroidism that usually accompanies renal failure. Derangements in parathyroid hormone secretion, calcium and phosphate metabolism, and renal production of 1,25-dihydroxycholecalciferol (the most active form of vitamin D) are all interrelated and pathogenetic features of renal osteodystrophy. Types of abnormalities detected radiologically vary with patient age, type of management, and duration of hemodialysis, as well as with techniques and type of film used and interest of the radiologist. An x-ray film of the hands should always be made--it will show subperiosteal resorption in a large number of patients on dialysis. Prevention and management of renal osteodystrophy hinge on control of hyperphosphatemia and hypocalcemia.
Bone and Bones↗
Seasonal variations in urinary excretion of calcium and magnesium in healthy subjects and patients with renal calculus and chronic renal failure.
Renal excretion of calcium in healthy subjects and in patients with renal stones increases in the summer, as compared to the winter values. In patients with chronic renal failure calciuria shows no seasonal variations. No essential difference in the monthly excretion of magnesium in 24-hour urine has been found between healthy persons and patients with renal stones.
Adolescent↗
Drug administration in renal failure.
Renal failure impairs urinary excretion of drugs and may also modify drug action by alternations in protein binding, distribution, biotransformation and, possibly, by retention of active metabolites. Dialysis adds another variable by altering the blood levels of those drugs soluble in plasma water and therefore available for diffusion or ultrafiltration. Renal insufficiency clearly modifies decisions about the choice and dose of a wide variety of drugs. Although data are accumulating at a rapid rate, available information about the use of drugs in patients with kidney disease is rather limited. The following is a summary of recent information on the use of a variety of drugs frequently utilized in patients with impaired renal function. The guidelines presented here are not absolute, but they are intended to be practical and reasonable, based on current information for adult patients of average size with kidney disease.
Analgesics↗
Intrarenal hemodynamics in acute myohemoglobinuric renal failure.
Renal blood flow (RBF) and its distribution were measured in acute renal failure induced by glycerol injection to water-drinking rats and to rats chronically loaded with NaCl solution. Mean RBF and intracortical blood flow distribution of both water-drinking and saline-loaded rats at 24 h after glycerol injection were not different from those of control rats. Although chronic saline loading blunted the impairment of renal function caused by glycerol as evidenced by serum creatinine values, no differences in renal hemodynamics were noted. This suggests that changes in glomerular arteriolar resistance or glomerular permeability might be of greater importance in the reduction of glomerular filtration rate than are alterations of blood flow.
Acute Kidney Injury↗
Obstructive polyuric renal failure following renal transplantation.
In a previously nephrectomized patient with a well functioning renal allograft, acute renal failure with massive polyuria and hypertension developed. Relief of a periureteric obstruction resulted in rapid correction of all three. Pathogenesis of hypotonic polyuria is thought to be a defect in the collecting duct permeability to water, stimulating nephrogenic diabetes insipidus. Normal urinary dilution and acidification suggest intact function of the ascending loop of Henle and distal convoluted tubules. The quick reversal of polyuria and renal failure after obtaining relief of the obstruction suggest that both the decrease in the glomerular filtration rate and tubular dysfunctions are due to functional changes in the nephron rather than to organic damage, a possibility also borne out by the findings in a renal biopsy specimen showing normal glomeruli and intact tubular epithelial cells. Ureteric obstruction should be considered in any patient with renal failure and polyuria; it may be a correctable cause of hypertension.
Acute Kidney Injury↗
Exploring Potential Causality and Molecular Mechanisms between Heart Failure and Renal Failure: Insights from Mendelian Randomization Studies, the MIMIC-IV Database and the Gene Expression Omnibus Database.
UNLABELLED: Introduction: Heart failure (HF) and renal failure (RF) frequently coexist as cardiorenal syndrome, but their underlying causal mechanisms remain poorly defined. METHODS: This study applied Mendelian randomization (MR) using genome-wide association study (GWAS) datasets to investigate the causal effect of HF on RF. The inverse variance weighted method assessed causality, and summary-data-based MR (SMR) was used to identify therapeutic targets. Additional analyses included 211 gut microbiota traits and 1,400 serum metabolites. Validation was performed using the MIMIC-IV database. Transcriptomic data were analyzed to identify differentially expressed genes (DEGs) and key transcription factors (TFs). RESULTS: This study found that HF significantly increases the risk of RF (OR = 1.54, 95% CI: 1.07-2.23, p = 0.020). SMR analysis identified SURF1 and MAP3K11 as potential therapeutic targets for HF and RF. One gut microbiota genus and one serum metabolite showed causal associations with both diseases. MIMIC-IV data supported the HF-RF association (OR = 2.94, 95% CI: 2.81-3.07, p < 0.001). A total of 11 overlapping DEGs were enriched in the MAPK cascade, with RELA identified as a key TF. CONCLUSION: This study provides genetic and molecular evidence supporting a causal role of HF in RF, highlighting microbial, metabolic, and immune mechanisms as potential therapeutic targets. .
Humans↗
An epidemiologic study of renal failure. II. Acute renal failure.
A total community study of acute renal failure (ARF) was carried out in Israel. The mean annual incidence was 4.8/100,000, the risk being 50% higher in males than in females. It was found that ARF is due primarily to a multiplicity of factors and rarely to a single cause; the high mortality associated with ARF is related to the patient's basic underlying condition. The epidemiology of ARF results from a compilation of the various conditions leading to it, and would, therefore, vary according to the differential distributions of these conditions in the population.
Acute Kidney Injury↗
Resistance to acute renal failure afforded by prior renal failure: examination of the role of renal renin content.
In this study, rats recovering from glycerol-induced acute renal failure were found to be protected from mercury-induced nephropathy, and HgCl2 poisoning protected rats from developing myohemoglobinuric renal failure. In view of the widely disparate nature of the renal failure models used, refractoriness appears to relate to an altered sensitivity of the organism itself rather than reflecting resistance to a particular nephropathic challenge. Renal renin content of the rats at the time of rechallenge was normal or high, a finding which contrasts sharply with that of chronically saline-loaded animals which also are refractory to ARF but have a maximally suppressed renal renin content. Renal renin depletion is not essential to the prevention of acute renal failure in the rat.
Acute Kidney Injury↗
Metabolic bone disease in chronic renal failure. II. Renal transplant patients.
Trabecular vertebral bone of renal transplant patients was quantitatively compared with bone from normal individuals and dialyzed and nondialyzed patienets with chronic renal failure reported in detail in an earlier study. Long- and short-term transplant patients have increased bone resorption and mineralization defects similar to renal osteodystrophy in dialyzed and nondialyzed patients. However, in transplant patients the magnitude of resorption is greater, and bone volume tends to decrease rather than increase. Resorptive activity in transplant patients is maximal during the first year after transplantation. Bone volume decreases continuously for at least 96 months after transplantation. Only decreased bone volume correlated with success or failure of the renal transplant. Morphologic findings in this study correlate with other clinical and morphologic data to suggest that reduction in bone volume in transplant patients results from a combination of persistent hyperparathyroidism and suppression of bone formation by steroid therapy.
Adult↗
The role of tubular necrosis in the pathophysiology of acute renal failure.
Renal tubular function was evaluated in vitro by kidney slice uptakes of p-aminohippurate (PAH) and tetraethylammonium (TEA) at 24 and 48 h in water-drinking rats and at 24 h in chronic saline-loaded rats after induction of acute tubular necrosis (ATN) by HgCl2 and glycerol injection. Significant correlations between decrease tubular uptake of PAH and TEA and elevated serum creatinine levels were noted in both models of ATN in water- and saline-drinking rats. However, with the same degree of impairment of PAH and TEA uptakes the creatinine was significantly lower in saline-loaded rats than in water-drinking rats in both forms of ATN. The correlation between impaired tubular function and elevated creatinine suggests that tubular damage and glomerular filtration reduction might be pathophysiologically related in ATN.
Acute Kidney Injury↗
Renal hemodynamics in HgCl2-induced acute renal failure.
Renal blood flow (RBF), outer cortical blood flow (OC-rbf) and inner cortical blood flow were determined by the microsphere method in water-drinking rats and chronic saline-drinking rats at 3, 12 and 24 h after injection of HgCl2, 4.7 mg/kh body weight. RFB and OC-rbf were decreased in both groups at 3 h post HgCl2 injection. Persistent reduction of OC-rbf was noted in water-drinking rats at 12 and 24 h post HgCl2 even though the total RBF returned to normal by 24 h. These parameters were normal in chronic saline-drinking rats. Despite normal RBF in water-drinking and saline-drinking rats, serum creatinines were still signigicantly elevated 24 h post HgCl2. Therefore, alterations in total renal perfusion do not entirely account for the decreased renal function that occurs under these circumstances.
Acute Kidney Injury↗
Use of prazosin in management of hypertension in patients with chronic renal failure and in renal transplant recipients.
Prazosin was used in combination with other antihypertensive drugs in the successful management of hypertension in seven patients with chronic renal failure and six renal transplant recipients, also with chronic renal failure. The addition of small doses of prazosin (mean 3 mg/day) to the antihypertensive regimen produced significant falls in systolic and diastolic blood pressures in both the lying and standing positions. The standing blood pressures were significantly lower than the lying blood pressures during prazosin treatment. Neither the mean blood urea concentrations nor the mean plasma creatinine concentrations changed significantly during prazosin administration. Chromium-51 edetic acid clearances did not change significantly during prazosin treatment in the seven patients in whom it was measured. Severe symptomatic postural hypotension occurred in one patient a week after starting prazosin 3 mg/day. This hypotensive episode was associated with a transient and reversible deterioration in renal function. Another patient developed a rash while on prazosin but it was probably related to propranolol rather than prazosin. Prazosin is thus an effective antihypertensive drug in patients with chronic renal failure, and it may be used with a variety of other drugs. It should be used cautiously, however, since patients with chronic renal failure may respond to small doses, and significant postural falls in blood pressure may result. There was no evidence that the use of prazosin resulted in progressive deterioration in the residual renal function of the patients with chronic renal failure.
Adult↗
Letter: Aetiology of chronic renal failure and renal osteodystrophy.
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Calcium↗