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At least 19 recordsLinked to original sources
PubMed1979

Deposition of beta 1H globulin in kidneys of patients with immune renal disease.

Renal biopsies from patients with a variety of immune type renal diseases were examined by immunofluorescence for the presence of C3 and its control protein, beta 1H globulin. Deposits of beta 1H were found in every instance (21 of 21 biopsies) in which C3 deposits were observed, irrespective of the underlying disease resulting in the C3 deposits, including lupus nephritis, acute poststreptococcal glomerulonephritis, idiopathic membranous glomerulonephritis, and Goodpasture's syndrome. In no instance was beta 1H found independently of C3. As previously shown in in vitro systems, beta 1H also binds to C3, presumably C3b, during activation of the complement system in immunologically induced renal disease.

Anti-Glomerular Basement Membrane Disease↗
PubMed1975

Renal handling of beta2-microglobulin in experimental renal disease.

Renal extraction and urinary excretion of 125I-labelled beta2-microglobulin was studied in rats. The effect of ischaemic renal injury, experimental pyelonephritis, and unilateral nephrectomy was investigated. The tubular secretion of o-iodohippurate (OIH) was measured for comparison. The urinary excretion was calculated as the ratio between the clearance of protein and the glomerular filtration rate. The glomerular filtration rate was estimated as clearance of polyethylene glycol (PEG 1000). The renal arteriovenous concentration difference was lower for beta2-microglobulin than for PEG 1000 IN ALL THE EXperimental groups. In unilateral renal disease the beta2-microglobulin excretion of the intact kidneys was similar to that of the diseased kidneys. A significant differences was noted only after ischaemic renal injury. The same was found for OIH. After removal of the intact kidneys the excretion of beta2-microglobulin increased about 10-fold in pyelonephritic animals and 2- to 30-fold in animals with ischaemic renal injury. One hour after unilateral nephrectomy in normal animals the ratio increased about 50 per cent. The tubular secretion of OIH did not change noticeably. It is concluded that the glomerular filtration is a main step in the intrarenal catabolism of beta2-microglobin and that its urinary excretion is considerably influenced by a reduction in the functioning kidney mass.

Animals↗
PubMed1979

Immunohistologic findings in the glomerular crescents in various renal diseases.

Renal tissues from 37 patients with glomerulopathies involving glomerular crescents were investigated using an immunofluorescence technique. Immunohistologic findings revealed two kinds of crescents, those with fibrinogen deposits (active), and those without (inactive). The degree of IgG deposition in glomeruli with active crescents was much higher than in glomeruli with inactive crescents in acute glomerulonephritis (AGN) and chronic glomerulonephritis (CGN). Active crescents were observed only in biopsy specimens taken within three months after the onset of acute glomerulonephritis or the acute exacerbation of chronic glomerulonephritis. These findings suggest that in AGN and CGN active crescents occur in an earlier stage of glomerular lesions and a more active stage in the immunological process than inactive crescents. The significance of active crescents in SLE, diabetic nephropathy and nephropathy associated with rheumatic arthritis was not evaluated due to the small number of patients.

Acute Disease↗
PubMed1977

Zinc metabolism in renal disease and renal control of zinc excretion.

Serum zinc concentrations are decreased in patients with a variety of clinical disorders including cirrhosis, nephrotic syndrome and renal insufficiency. Urinary zinc excretions are increased in the first two disease states. Symptoms of acute zinc deficiency (anorexia, dysfunction of smell and taste, and mental and cerebellar disturbances) and chronic zinc deficiency (growth retardation, anemia, testicular atrophy, and impaired wound healing) are common in these patients. It remains unresolved whether these disease states are indicative of true symptomatic or asymptomatic zinc deficiency or merely reflect a decrease in available zinc binding proteins. The low serum zinc concentrations and high urinary zinc excretions in patients with nephrotic syndrome do not appear to be due to loss of zinc bound to urinary proteins. Studies in dogs indicate increased serum and urine concentrations of certain amino acids(cysteine, histidine) greatly increase urinary zinc excretions. Studies are now underway to determine if the hyperzincuria and hypozincemia of cirrhosis, nephrotic syndrome and hyperalimentation can be explained by an increase in these urinary amino acids.

Animals↗
PubMed1977

Quantitation of renal antigen excretion in the urine of normal children and of children with various renal diseases. I. Quantitation of renal antigens in random urine samples.

This study reports a serologic method for the measurement of kidney-derived antigens in the urine of healthy children and of children with renal diseases. Two hundred twenty patients were studied. Four groups were recognized: group A, patients with no evidence of renal disease; group B, patients with past history of active urinary tract infection; group C, patients with active urinary tract infection; group D, patients with other renal diseases. Urinary renal antigen concentration was tested by the complement fixation method, in which titers of antigens in the urine were compared with a standard human renal antigen extract. The distribution of renal antigen concentrations in group C differed significantly (P(X2Y less than 0.001) from the other three groups. About 85% of patients in groups A, B, and D had levels below 0.6 mg/ml, whereas in group C only 53% of patients had similar concentrations. After factoring the results by the urinary concentration of creatinine, 85% of patients in group C had antigen levels above 0.6 mg/ml as opposed to 24%, 44%, and 27% in groups A, B, and D, respectively. The results of the study are consistent with the assumption that the rate of discharge of renal antigenic material in the urine is accelerated in certain renal diseases.

Antigens↗
PubMed1977

Salivary antipyrine kinetics in hepatic and renal disease and in patients on anticonvulsant therapy.

The effects in man of liver disease, renal failure and hepatic microsomal enzyme induction on the elimination kinetics of antipyrine in saliva have been examined. Antipyrine (10 mg/kg) was given orally and assayed in saliva by gas-liquid chromatography. The mean antipyrine half-life from saliva in nine epileptic subjects receiving long term anticonvulsant drug therapy (6 hr +/- 0-9 SEM) was significantly shorter than in twenty normal healthy volunteers (10-7 +/- 0-6). Therapy included phenytoin and phenobarbitone, two drugs known to induce hepatic microsomal enzymes. Five subjects with chronic renal failure exhibited no significant difference in salivary anti-pyrine half-life (11-7 +/- 1-9) compared to the control group, whereas six subjects with chronic liver disease and impaired hepatic function had significantly increased half-life values (42-4 +/- 10). The results suggest that differences in the activity of hepatic microsomal enzymes are reflected by changes in salivary antipyrine elimination kinetics. Chronic renal failure appeared to have no effect on the function of these enzymes.

Adult↗
PubMed1977

Heroin addiction and renal disease.

In this paper, renal involvement secondary to other medical complications of heroin addiction is discussed. We review 12 published studies totalling 102 heroin addicts with renal disease. Of these, in only 40 patients could other discernible causes of renal disease be excluded. The existence of 40 reported cases of renal disease from a population of more than half a million is insufficient data upon which to postulate the existence of a type of renal disease unique to heroin addicts.

Adolescent↗
PubMed1979

Evaluation of a new method for treating segmental renal disease.

Experimental segmental renal artery embolization was performed to evaluate the feasibility of therapeutic segmental renal embolization. In group 1, a two kidney dog model, segmental embolization of the right kidney was performed in ten dogs using Gelfoam, Silastic elastomer and barium sulfate. In group 2, a one kidney dog model, segmental embolization of left kidney was performed using Gelfoam and Silastic elastomer. In the remaining three dogs of group 2, embolization was not done for control. Sequential blood pressure measurements, plasma renin activities and renal arteriograms were obtained. Three dogs in group 2 died following unintentional complete renal embolization. Seventeen of the 18 dogs of the entire study remained normotensive after embolization. One dog had persistent hypertension develop which was controlled by a second, total renal embolization. The results suggest that therapeutic segmental renal embolization is a feasible method for treating segmental renal disease.

Aneurysm↗
PubMed1978

Cerebral transmitter precursors and metabolites in advanced renal disease.

Patients with chronic renal disease had low plasma total tryptophan but an abnormally high proportion of this was in the free state. The subjects with encephalopathy had raised plasma free tryptophan, CSF tryptophan, and CSF 5-hydroxyindoleacetic acid. CSF tryptophan correlated better with plasma free than with plasma total tryptophan. Plasma and CSF tyrosine concentrations were normal but CSF homovanillic acid was raised especially in subjects with encephalopathy. The possible significance of these changes in advanced renal disease is discussed.

Adult↗
PubMed1977

Nutritional implications of renal disease. IV. Nutritional aspects of chronic renal insufficiency in childhood.

Nutritional treatment of children with renal insufficiency presents special problems related to undernutrition, i.e., insufficient caloric intake to permit normal growth, vitamin D intake, and protein needs, as well as depressed appetite. With regard to energy, it is suggested that uremia may lead to increased caloric requirements, thus exacerbating growth depression. Protein requirements, which actually may not be as important as caloric needs, have not been determined for uremic children. Another factor in growth failure in such children involves vitamin D metabolism and its role in renal osteodystrophy. Successful dietary management of these various interrelated aspects of childhood renal disease requires sensitive, knowledgeable personnel.

Acidosis↗
PubMed1979

Grand rounds: Nashville VA Hospital--Vanderbilt University. Saturday conference: renal disease in the juvenile diabetic.

Renal disease, particularly glomerulosclerosis, is a major cause of morbidity and mortality in patients with juvenile-onset diabetes mellitus. Signaled by the onset of proteinuria after 15 or more years of insulin therapy, progressive renal insufficiency due to glomerulosclerosis terminates in uremia within five years. Although some patients have benefited from chronic dialysis programs, the outcome in uremic diabetics has been considerably better if successful renal transplantation can be accomplished. Extrarenal complications of diabetes mellitus and recurrence of diabetic lesions in transplanted kidneys have hampered the recovery and rehabilitation of transplant recipients. Other renal diseases encountered in juvenile diabetics are reviewed.

Acute Kidney Injury↗
PubMed1978

Nutritional inhibition of genetically determined renal disease and autoimmunity with prolongation of life in kdkd mice.

Striking inhibition of development of renal disease and prolongation of lifespan have been achieved in kdkd mice by restricting their daily food intake. Restricting protein intake alone did not prolong life nor did it inhibit development of kidney disease. The kdkd nephronophthisis, although very different histologically from the renal disease of B/W mice, may also have immunological components. Like the immunologically based renal disease of B/W mice, renal disease in kdkd mice is decreased or eliminated histologically by dietary restriction, which inhibits development of autoimmunity directed toward the erythrocytes of these mice. Further analysis will be needed to elucidate the cause of progressive renal disease in both the kdkd and B/W models and to permit understanding of the profound influence of restriction of food intake on development and progression of these very different renal diseases.

Animals↗
PubMed1979

Drug-induced renal disease.

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.

Acute Disease↗
PubMed1977

Studies on serum lipoproteins in renal diseases.

Serum lipoproteins of 25 patients with uncomplicated renal diseases were studied with polyacrylamide gel block electrophoresis. (1) In the nephrotic syndrome (or nephrotic phase of nephritis), marked increases of chylomicrons, pre-beta lipoprotein or beta lipoprotein and decreases of alpha lipoproteins were detected in the most of the patients. Qualitative change was also frequent as in the glomerulonephritis. (2) In the renovascular hypertension, metabolism of serum lipoproteins was involved also. The principal abnormality was in alpha lipoproteins including the lipid-loaded albumin. Marked increases of alpha lipoproteins, to the level equal to or more than beta lipoprotein, was detected in 2 of 3 patients studied in this period. Surgical correction of abnormal physiology had resulted in a return to a normal lipoprotein profile. (3) In the glomerulonephritis confirmed by biopsies, serum lipoprotein abnormalities were detected more frequently than in the reported past studies as analyzed with the method employed in this study. Qualitative as well as quantitative abnormalities were in beta lipoprotein and alpha lipoproteins in the early and middle phase of the disease process. Gross qualitative change occured frequently. Furthermore, lipoprotein abnormalities in renal diseases were reversible; i.e., when the disease had ameliorated or was corrected surgically, the lipoprotein profile returned to the normal or near-normal profile. In conclusion, the results of the present study indicated that serum lipoprotein disorders are involved in the disease process of three major clinical entities of the renal diseases.

Adolescent↗
PubMed2026

Genome-wide DNA methylation analysis revealed epigenetic mechanism underlying end-stage renal disease.

End-stage renal disease (ESRD) remains a major clinical challenge with high morbidity and mortality, and its molecular mechanisms, particularly those shared among diverse primary kidney diseases during progression to ESRD, have not been studied. Here we conduct a large-scale two-stage epigenome-wide association study of ESRD in two independent cohorts consisting of 704 controls and 1031 ESRD cases. We identify 52 ESRD-associated differentially methylated CpG positions (ESRD DMPs) showing consistent association between the two cohorts and across diverse kidney diseases, implicating 144 candidate genes enriched in inflammatory and immune pathways. Five of the 52 DMPs are associated with ESRD complications, and seven with renal function decline in early-stage chronic kidney disease, demonstrating their potential as prognostic biomarkers for ESRD and its complications. Our findings highlight inflammation, immune dysregulation, and renal fibrosis as shared epigenetic drivers of ESRD progression, and identify biomarkers with potential utility for risk stratification and therapeutic intervention.

Humans↗
PubMed1977

On-line computerized data handling system for treating patients with renal disease.

Some patients with renal disease accrue 6,000 to 8,000 individual data items relating to symptoms, signs, laboratory information, and treatment in one year. To deal with the problem of handling so many data items, the following steps were taken: (1) a dictionary of terms peculiar to nephrology was created; (2) manual time-oriented records for nephrology were constructed; and (3) an on-line data processing system, using a PDP-11/70 computer and remote teleprocessing terminal, was developed. On the terminal screen, up to 11 consecutive patient visits can be displayed horizontally, with 18 data items displayed vertically. Up to 30 of the most recent patient visits are easily accessible. For patient treatment, a special feature allows a rearrangement and instantaneous display of any combination of data, thus permitting review of essential feedback relationships between clinical events and treatment.

Data Display↗