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At least 19 recordsLinked to original sources

PubMed1991

NCI-Black-Reiter (NBR) male rats fail to develop renal disease following exposure to agents that induce alpha-2u-globulin (alpha 2u) nephropathy.

The NCI-Black-Reiter (NBR) rat is the only strain of male rat known not to synthesize the hepatic form of the low molecular weight protein, alpha 2u-globulin. In previous studies, NBR rats were shown not to develop renal disease when exposed to decalin, a compound known to induce alpha 2u-globulin nephropathy in other rat strains. The objective of this study was to show that the presence of alpha 2u-globulin (alpha 2u) is essential for the development of this syndrome in rats exposed to 2,2,4-trimethylpentane (TMP), 1,4-dichlorobenzene (DCB), isophorone (IP), PS-6 unleaded gasoline (UG), and d-limonene (d-L). The induction of alpha 2u-nephropathy in F344 male rats with lindane was used as a positive control and this response was contrasted to male NBR and female F344 rats treated with lindane. Five to seven 11-week-old male NBR rats were exposed to TMP (500 mg/kg/day), DCB (500 mg/kg/day), IP (1000 mg/kg/day), UG (500 mg/kg/day), d-L (1650 mg/kg/day), or lindane (10 mg/kg/day) and five 11-week-old male and female F344 rats were exposed to lindane (10 mg/kg/day) by oral gavage on 4 consecutive days. NBR male and F344 male and female rats gavaged with corn oil were incorporated in the study as vehicle controls. The presence of hyaline droplets was assessed in perfusion-fixed kidneys by staining paraffin sections with Mallory-Heidenhein stain and in GMA sections with Lee's methylene basic blue fuchsin stain. Paraffin sections were also analyzed immunohistochemically for the presence of alpha 2u. Under exposure conditions that clearly induce alpha 2u-nephropathy in male F344 rats, no lesions, hyaline droplets, or alpha 2u were detectable in treated or control male NBR and female F344 rats. It is thus concluded that the presence of alpha 2u is causal to the development of renal disease in rats exposed to TMP, DCB, IP, UG, d-L, and lindane.

Alpha-Globulins↗

PubMed1991

N-myc oncogene expression in porcine renal development and oncogenesis.

N-myc oncogene expression was characterized in porcine kidneys to investigate the potential role of this gene in normal renal development and oncogenesis. N-myc RNA expression was detected in porcine kidneys from birth until 5 wk of age, which corresponds to the time when glomerular differentiation is completed. Immunohistochemical studies revealed that N-myc protein was selectively expressed in the primordia of renal proximal tubule epithelial cells. These cells were cultured in vitro and continued to express N-myc for a limited time. Comicroinjection of a mutant ras oncogene and N-myc into these cells led to focus formation in soft agar, loss of contact inhibition, and the establishment of an immortalized cell line. These findings support a multistep model of renal oncogenesis that involves overexpression of N-myc.

Animals↗

PubMed1990

Efficacy of calcium carbonate and low-dose vitamin D/1,25(OH)2D3 in reducing the risk of developing renal osteodystrophy in children on continuous ambulatory peritoneal dialysis.

Eight children with terminal renal insufficiency on continuous ambulatory peritoneal dialysis were followed for 12 months to evaluate laboratory parameters of mineral ion and bone metabolism. Calcium carbonate (range 47-295 mg/kg body weight per day) was given in combination with low doses of either vitamin D or 1,25(OH2D3. Blood urea nitrogen and serum phosphate concentrations remained well controlled throughout the observation period. A significant increase in serum calcium levels from 2.35 +/- 0.18 to 2.61 +/- 0.22 mmol/l (mean +/- SD) was observed during the first 6 months. Alkaline phosphatase activity and mid-C-regional parathyroid hormone, both indirect parameters of bone metabolism, revealed no evidence of severe secondary hyperparathyroidism. Our data indicate that calcium carbonate may be sufficient to induce relative hypercalcaemia in uraemic children, and thus reduce the risk of developing renal osteodystrophy. Unwanted side-effects of vitamin D preparations, i.e. increased intestinal phosphate absorption and hypercalcaemia after successful renal transplantation, may thus be avoided.

Administration, Oral↗

PubMed1990

Developing renal innervation in the spontaneously hypertensive rat: evidence for a role of the sympathetic nervous system in renal damage.

The spontaneously hypertensive rat (SHR) exhibits increased renal sympathetic nerve activity and neurotransmitter levels compared with the control Wistar-Kyoto rat (WKY). These renal nerve abnormalities have been implicated as the cause of hypertension in the SHR. The aims of the present study were to characterize the ontogeny of renal sympathetic innervation in SHR in order to determine any functional implications. Glyoxylic acid histofluorescent and radio-enzymatic norepinephrine assays demonstrated an accelerated development of renal innervation in newborn and 1-, 2-, 3- and 6-week-old SHR compared with WKY. Sympathetic nervous system function was blocked in developing male SHR by treating pups from days 0 to 14 with: (1) guanethidine, (2) combined alpha- and beta-receptor antagonists (prazosin and timolol), or (3) vehicle (5% sucrose). Blood pressure (mean), renal function (plasma creatinine) and histologic renal damage were assessed at 42 weeks of age. Although the blood pressure of the drug-treated rats remained elevated, renal damage was reduced and renal function was improved compared with control (sucrose-treated) SHR. The data demonstrate that the SHR kidney develops a precocious sympathetic innervation and that inhibition of the development of sympathetic function ameliorates renal damage independently of systemic hypertension.

Animals↗

PubMed1979

The effects of maternal protein deprivation on renal development and function in neonatal rats.

This study was undertaken to investigate the effects of pre- and/or postnatal maternal protein deprivation (PD) on renal functional development in the offspring. Pregnant rats were fed either a control (24% protein) or low (8 or 10%) protein diet during gestation and lactation. Progeny of these dams were cross-fostered at birth, yielding four experimental groups: pups born of control dams and nursed by PD or control dams and pups born of PD dams and nursed by control or PD dams. While the effects of prenatal PD on body and kidney growth were negligible, PD during the nursing period appeared to have a more profound effect on body and kidney weight. Renal transport functions, quantified in vitro, were differentially affected by these dietary manipulations. Renal transport capacity for organic acids and bases was depressed in pups nursed by PD dams. Maturation of the renal organic acid transport system was also delayed in these pups. alpha-Aminoisobutyric acid accumulation by renal cortical slices was enhanced only in 10-day old rats stressed by pre- and postnatal maternal PD. Renal gluconeogenic and ammoniagenic capacity was not impaired by these dietary manipulations. No differences in protein or water content of renal cortical slices were observed.

Aminoisobutyric Acids↗

PubMed1992

Cellular and molecular mechanisms of renal development and tubulogenesis.

Recent advances in the basic mechanisms of developmental biology have started to shed new light on the mechanisms of nephrogenesis. The kidney is the only epithelial organ that starts as mesenchyme and converts to epithelium. It appears that the mesenchyme is composed of stem cells that are able to form glomeruli and proximal and distal tubules under the inductive influences of the ureteric bud. Epithelial cells cultured in a three-dimensional matrix could be induced to form tubules under the influence of a soluble factor from fibroblasts. This factor was identified as scatter factor or hepatocyte growth factor. Polycystic kidney disease appears to be a developmental renal disease in which a basolateral protein, the Na/K ATPase, is mistargeted to the apical and lateral membranes.

Animals↗

PubMed1992

Hyperaminoaciduria identifies patients at risk of developing renal tubular toxicity associated with ifosfamide and platinate containing regimens.

We monitored renal tubular function in 18 neuroblastoma patients treated with chemotherapeutic regimens containing Ifosfamide and platinates. The total IFO dose ranged from 30 to 48 g/m2. After each IFO course and at regular intervals during follow-up 24 hour urinary exception of aminoacids, qualitative excretion of protein and glucose, tubular reabsorption of phosphate, serum pH, and liver enzyme (SGOT and SGPT) were measured. The ratio of alpha-amino-Nitrogen/total-Nitrogen (normal less than 2.5%) and the urinary excretion pattern were used to quantify the aminoaciduria in 12 out of 15 evaluable patients some degree of tubular toxicity occurred during treatment, slowly progressing to a Debré-de Toni-Fanconi syndrome (DTFS) in 7 patients. The DTFS was fully developed in most cases 3-9 months after the end of treatment and was reversible in 3 cases. Hyperaminoaciduria (HAA) occurred in all patients during treatment, preceding other signs of tubular toxicity. The maximum ratio measured before development of a DTFS was significantly higher in the patients with severe toxicity (P less than .01). HAA characterized by a ratio greater than 10% predicts the development of a DTFS with a sensitivity of 71.4% and a specificity of 87.4%.

Alanine Transaminase↗

PubMed1992

The effect of intrauterine growth retardation on the development of renal nephrons.

OBJECTIVE: To investigate the effect of Type II (asymmetrical) intrauterine growth retardation (IUGR) on renal development. DESIGN: A prospective descriptive study. SETTING: Department of Fetal and Infant Pathology, Liverpool Children's Hospital. SUBJECTS: Six (severely) affected IUGR stillbirths of known gestational age with a control group of stillbirths with birthweight greater than 10th centile, and eight liveborn IUGR infants who died within a year of birth with a control group of appropriately grown infants who died within a year of birth (postnatal groups). TECHNIQUES: The kidneys from all the groups studied were analysed using unbiased, reproducible and objective design-based stereological techniques. MAIN OUTCOME MEASURES: Total renal nephron (glomerular) numbers and average volumes of total nephron and cortical and medullary nephron segments. RESULTS: Nephron number estimates lay below the control group's 5% prediction limit in five out of the six growth-retarded stillbirths, and were significantly (P less than 0.005, IUGR at 65% of the control mean) reduced in the postnatal group. Estimates of nephron (segment) volume did not differ between control and IUGR groups. CONCLUSIONS: Type II intrauterine growth retardation may exert a profound effect on renal development. The reduced nephron number at birth, together with the lack of any early postnatal compensation in either nephron number or nephron size, emphasizes the need for vigorous antenatal surveillance for IUGR and consideration of elective preterm delivery of affected fetuses. A systematic review of other organs, which develop in a similarly rapid fashion during the late intrauterine period, is indicated by this work. With one exception, all birthweights in the growth-retarded groups were below the third centile, thus the precise quantitative relation between progressive IUGR and renal function requires further assessment.

Birth Weight↗

PubMed1990

N-linked oligosaccharides during human renal organogenesis.

The structure of fucosylated derivatives of N-acetyl lactosamine expressed during human renal development has been studied by the combined use of monoclonal antibodies and glycosyl hydrolases. LeX is expressed on the ureteric bud ampulla carried N-linked on a glycoprotein. It is also present in the proximal tubule as a ganglioside. H-Type II substance is expressed on the endothelium of the developing renal vasculature. It is also carried N-linked to a glycoprotein. These regulated changes in the cell surface carbohydrate expression are important in understanding cell interactions and receptor systems during renal development.

Antibodies, Monoclonal↗

PubMed1977

Retarded development of fetal renal alkaline phosphatase in mice given 2,4,5-trichlorophenoxyacetic acid.

Histologic study of the fetal offspring of maternal mice given 2,4,5-trichlorophenoxyacetic acid (2,4,5-T) suggested that the previously reported fetal "cystic kidneys" were due to a retardation in fetal renal development and downgrowth of the renal papilla into the pelvis. To determine a possible retardation in renal alkaline phosphatase or functional development, maternal mice received by gavage 60-120 mg/kg, 2,4,5-T on days 6-14 of pregnancy. At necropsy on day 17, the fetal kidneys were excised and fixed 24 hr in cold 65% ethanol. Paraffin sections stained by Gomori's method revealed alkaline phosphatase mainly in tubules in the inner renal cortex. Fetal kidneys showing diminished or no alkaline phosphatase were designated subnormal. There was a statistically significant greater incidence of subnormal fetal kidneys in the 2,4,5-T-treated mice than in the untreated controls. In three experiments, some mice were also sacrificed on day 18, and the incidence of subnormal fetal kidneys was significantly lower than on day 17. This retardation in renal alkaline phosphatase development indicates a retardation in renal functional development and indirectly supports the view that 2,4,5-T also retards the morphological development of the fetal kidney and is not a renal teratogen in mice. It also illustrates that selected histochemical studies may be helpful in a teratologic investigation.

2,4,5-Trichlorophenoxyacetic Acid↗

PubMed2025

Zonal endothelial cell heterogeneity underlies murine renal vascular development.

The renal vasculature consists of highly specialized blood vessels with distinct physiological functions. Defining their transcriptional signatures and tracing their developmental ontogeny has thus far been challenging due to a lack of regionally specific endothelial biomarkers. Here, we performed single nuclear RNA sequencing (snucRNA-Seq) to interrogate the transcriptional heterogeneity of embryonic renal endothelial cells (ECs). We identified ten endothelial subtypes, and validated regionally restricted expression of novel marker genes of glomeruli, arteries, vasa recta, and immature capillary subtypes using multiplex RNAscope. We also define previously uncharacterized and heterogeneous molecular signatures of the immature renal vasculature, including putative endothelial progenitors. We interrogate biological characteristics of immature EC types using a variety of in vivo tools. Lineage tracing of Esm1-expressing cells reveals the previously unrecognized multi-origin and multi-clonal endothelial tip cell contribution to the glomerular vasculature. Together, this study provides a validated, tool-focused developmental atlas of the murine renal vasculature and elucidates novel cellular mechanisms of nephron vascularization.

Animals↗

PubMed1992

Late development of renal carcinoma in allograft kidney.

The Cincinnati Transplant Tumor Registry recorded 169 cases of renal carcinoma developing in transplant recipients. The great majority of these cases were of primary renal cell carcinoma developing in the recipient native kidneys. Renal carcinoma developing de novo in the renal allograft occurred 17 times, with a maximal interval to clinical development of 85 months after transplantation. The development of multicentric renal cell carcinoma in an allograft 156 months after transplantation is described. The 24-year-old white male recipient with Alport's syndrome received a cadaver renal allograft from a healthy 27-year-old black man who had died of a cerebral hemorrhage in 1977. At 13 years after transplantation the recipient had upper abdominal pain. Ultrasound revealed 2 incidental renal masses and a renal cyst in the allograft. Partial nephrectomy confirmed the presence of multicentric renal carcinoma. The graft was left in situ and immunosuppression was maintained. The recipient continued to do well with no evidence of disease 1 year postoperatively. Deoxyribonucleic acid banding demonstrated that the tumor and recipient blood were of different patterns.

Adult↗

PubMed1992

Development of renal hemodynamics: glomerular filtration and renal blood flow.

The regulation of RBF and GFR is essential to understanding renal physiology during mammalian development. Without this knowledge, clinical judgment regarding overall renal function in human neonates, especially those considered high risk, is reduced to guesswork. The plethora of reports in which assessment of RBF and GFR were attempted have provided a legacy purporting the neonatal kidney as immature, inadequate and dysfunctional--nothing could be farther from the truth. Our failure to understand kidney function in the neonate does not justify shifting the blame for unwanted disturbances in fluid and electrolyte balance, metabolic acidosis, and azotemia to a small kidney. After a critical stage of renal development has been reached, subsequent changes in RBF and GFR are only quantitatively different from the adult kidney.

Animals↗

PubMed1991

Development of renal failure in children with the prune belly syndrome.

From 1970 to 1987, 32 male and female patients with the prune belly syndrome were evaluated. Of these patients 11 died as neonates or infants, and autopsy in 9 revealed 6 cases of diffuse and severe renal dysplasia. In the 10 surviving patients renal insufficiency developed and a total of 13 nephrectomies and renal biopsies were performed. Renal dysplasia was noted in 9 specimens, but unlike the infant kidneys, the dysplastic changes involved less than 25% of the parenchyma in most cases. Renal failure in these 10 patients was caused by pyelonephritis and obstruction. In our estimation perinatal renal failure in patients with the prune belly syndrome results from renal dysplasia caused by an in utero insult, while in older patients pyelonephritis and obstruction are the causes. Careful treatment of reflux, obstruction and urinary tract infections may decrease the incidence of renal failure in patients with the prune belly syndrome who survive infancy.

Adult↗

PubMed1990

Counterbalance in functional adaptation to ureteral obstruction during development.

Renal counterbalance, as described by Hinman in 1923, is the phenomenon of increased function of the intact kidney in proportion to the loss of function resulting from unilateral ureteral obstruction (UUO). In the neonatal guinea pig, chronic partial UUO results in severe vasoconstriction and growth arrest of the ipsilateral kidney. Angiotensin II appears to contribute significantly to the vasoconstriction, and the renin-angiotensin system is also involved in the hemodynamic response of the intact opposite kidney to UUO and to relief of UUO. Immunolocalization of renin following complete UUO in the neonatal rat revealed extension of renin-containing cells along the length of the afferent arteriole in both the obstructed and the intact opposite kidney. The proportion of juxtaglomerular apparatuses with detectable renin and renin messenger ribonucleic acid (mRNA) (identified by in situ hybridization), as well as renal renin content (a measure of active renin), were increased in the obstructed kidney compared with the intact opposite kidney. Chemical sympathectomy by chronic guanethidine administration reduced the total renin mRNA in the obstructed kidney (determined by Northern blot analysis) and prevented the increased renin immunostaining in both kidneys. Thus, renal counterbalance in the developing kidney subjected to UUO is mediated or modulated by the renal nerves and involves marked alterations in gene expression and cellular processing of renin.

Humans↗

PubMed1990

[A study of the native kidneys in patients with chronic renal failure. Report 2: Correlation between cystic changes in native kidneys and development of renal tumor].

The factors which made acquired cysts develop to renal tumors in chronic hemodialysis patients was investigated from clinical and histological findings. Although three renal tumors were found among 151 patients with chronic renal failure, clinically, one case had acquired cystic disease of the kidneys (ACDK), one case had simple cysts and the other case did not have any cyst. However, the last two cases had multiple small cysts histologically. In ACDK, renal tubules were degenerated and dilated, fused to each other, forming more larger cysts. Furthermore, epithelium of acquired cysts showed columer and dysplastic change, and papillary adenomas were developed into the inner space of the cyst wall. And ACDK kidney without renal tumor also revealed the same findings in histological examinations. It was postulated that renal tumor occurred from the papillary projections of the dysplastic epithelium of cysts. Therefore cysts in uremic patients seemed to be different from the simple cyst in normally functioning kidneys.

Adult↗

PubMed1976

Development of renal scarring in an adult with recurrent urinary tract infection.

An adult patient is described with recurrent urinary tract infections who developed renal scarring while under observation. Intravenous urography (I.V.U.) and renal arteriography were performed during an initial attack of pyelonephritis and I.V.U.s were repeated at intervals during follow-up, when the patient was having recurrent infections. Over 2 years the right kidney size diminished from 10.5 to 7.0 cm, the cortex became irregular and calyceal clubbing occurred. During a further 2 years, when on regular treatment, attacks became less frequent but left-sided symptoms predominated. Repeat I.V.U. at the end of this period showed that the left kidney size had reduced from 12 to 10 cm, again with the development of cortical irregularity and calyceal clubbing. Biochemical evidence of renal impairment developed. At no time were obstruction, reflux or associated pathology demonstrated and there was no history of analgesic abuse. Recurrent infection is suggested as the etiology of the scarring.

Angiography↗

PubMedDate not supplied

[Mechanism of the therapeutic effect of furosemide and mannitol in hemorrhagic shock and developing acute renal insufficiency].

Acute hypotension leads to the development of anuria, almost complete stoppage of the cortical nephron filtration with blood retransfusion failing to restore the upset functions. But against background of preliminary administered diuretics the blood retransfusion renews filtration and restores diuresis. Preliminary administration of diuretics prevents collapse of the proximal tubules, their administration after blood losses increases the tubular pressure and prevents obstruction of the nephron. Under the effect of diuretics the oxygenation of deep-seated segments of the kidney substantially gains in strength due to an increasing renal blood circulation and diminished vasoconstriction. Diuretics increase the oxidative phosphorylation in the cells of the renal epithelium, help augment accumulation of calcium by renal mitochondria and prevent the development of irreversible hypoxic shifts. Combined administration of furosemide and mannitol represents an effective means of prevention and early treatment of acute renal insufficiency.

Acute Kidney Injury↗