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Results for “Kidney fibrosis”

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At least 19 recordsLinked to original sources

PubMed1977

Gray scale ultrasonography in medullary cystic disease of the kidney and congenital hepatic fibrosis with tubular ectasia: new observations.

The gray scale ultrasound findings of three patients with medullary cystic disease of the kidney and two patients with congenital hepatic fibrosis with tubular ectasia are reported. Medullary cystic disease of the kidney typically presents early in adulthood with renal failure and salt-losing nephropathy. The spectrum of gray scale ultrasound findings in this entity includes irregular widened central echoes when small cysts are present and well defined cystic structures when larger medullary cysts are the predominant lesion. The ultrasound findings in congenital hepatic fibrosis with tubular ectasia seem to be a characteristic combination of nephromegaly, a distorted renal echo pattern, and high level echoes in the liver. Ultrasound is a useful noninvasive method which is complementary to other methods in the identification and differential diagnosis of bilateral renal cystic disease.

Adult↗

PubMed1977

Congenital hepatic fibrosis, liver cell carcinoma and adult polycystic kidneys.

In reviewing the literature, we found no liver cell carcinoma (LCC) or well-documented adult polycystic kidneys (APK) associated with congenital hepatic fibrosis (CHF). We report a 69-year-old man with CHF, LCC, APK, duplication cyst of distal portion of stomach, two calcified splenic artery aneurysms, myocardial fibrosis and muscular hypertrophy of esophagus. The LCC was grossly predunculated and microscopically showed prominent fibrosis and hyaline intracytoplasmic inclusions in the tumor cells.

Aged↗

PubMed1977

[Congenital hepatic fibrosis and polycystic disease of the kidneys in two siblings (author's transl)].

Report of 2 siblings, aged 12 1/2 and 9 years, with congenital hepatic fibrosis and polycystic disease of the kidneys. Hepatosplenomegaly had been noted in both children at birth. The younger child had suffered from oliguria aged 2 1/2 years. At diagnosis both children had low platelet counts, one also had leucopenia. The cystic disease of the kidneys was verified by angiography. Coeliacography and splenopartography were diagnostically irrelevant. The diagnosis only became apparent from liver biopsy which was performed during splenectomy. After splenectomy there was an increase of platelets, white blood cells and the clotting factors II, V and X. The three years follow-up showed a constancy of renal impairment and of the minor oesophageal varices observed in the one patient who did not have a spontaneous spleno-renal anastomosis. So far no bleeding has been observed. Porto caval anastomosis was omitted in both children. Pros and cons are being discussed.

Child↗

PubMed2026

Small extracellular vesicles are the key players in ochratoxin A-induced kidney toxicity.

BACKGROUND: Despite growing evidence of ochratoxin A (OTA)-induced kidney toxicity, the underlying mechanisms remain elusive. Emerging evidence suggests that small extracellular vesicles (sEVs) act as mediators of intercellular communication to recipient cells during various physiological and pathological conditions. Given the distinctive properties of sEVs, it is hypothesized that OTA-induced sEVs might mediate the OTA-induced kidney pathogenesis. METHODS: To explore the involvement of sEVs in OTA-induced kidney toxicity, sEVs were isolated and characterized from OTA-exposed rat kidney epithelial cells (NRK52E). Later, these sEVs were used to treat NRK52E cells and Wistar rats to assess the impact of OTA-induced sEVs on kidney toxicity. Label-free proteomics was also performed on OTA-induced sEVs, and key proteins were identified and validated. The biodistribution of sEVs in rats was also assessed using live imaging. The role of validated protein/s in kidney toxicity was further confirmed via a gene silencing and overexpression study. RESULTS: OTA exposure increased sEV secretion into conditioned media of NRK52E cells and into the urine of Wistar rats. Interestingly, we found that OTA-induced sEVs cause similar kidney toxicity in vitro and in vivo systems as OTA exposure, and blocking of sEV secretion markedly alleviated OTA-mediated kidney toxicity. Proteomics analysis identified annexin A2 and fibrinogen-ɣ as common proteins detected in sEVs derived from OTA-exposed NRK52E cells or rat urine. However, immunoblotting validated that annexin A2 was the only sEV-associated protein, expressed significantly in both NRK52E and rat urine following OTA exposure. Notably, silencing of annexin A2 attenuated the ability of OTA-induced sEVs to cause kidney toxicity, whereas overexpression exacerbates it. CONCLUSIONS: Our findings identify the annexin A2-enriched sEVs as key mediators of OTA-induced kidney toxicity. Annexin A2, along with other kidney injury markers, offers a promising non-invasive translational biomarker for early detection and monitoring of OTA-induced kidney toxicity.

Ochratoxins↗

PubMed1976

Peritoneoscopy in adult polycystic kidney disease: its diagnostic value.

The value of peritoneoscopy in the diagnosis of renal polycystic disease was tested in nine patients with adult polycystic disease and one with congenital hepatic fibrosis. The right kidney was visualized in all ten cases and the left in seven. Renal cysts were recognized by peritoneoscopy in eight of the ten patients. Factors impeding visualization of the kidneys and the cysts were: a) fixation of the splenic flexure of the colon; b) non-superficial renal cysts. Of six cases in which intravenous pyelography was not diagnostic, peritoneoscopy was positive in four. No correlation was found between the degree of hepatic and renal cystic involvement.

Adolescent↗

PubMed1977

Spontaneous glomerulonephritis in dogs. II. Correlation of glomerulonephritis with age, chronic interstitial nephritis and extrarenal lesions.

A morphologic study of 103 dogs, including two with renal amyloidosis, showed that different types of diffuse glomerulonephritis are correlated with different age groups. Membranous and membranoproliferative glomerulonephritis were more common in middle-aged and older animals, whereas mesangial lesions were found predominantly in younger dogs and considered to be early glomerular changes. Glomerulonephritis largely occurred independently of interstitial nephritis. The incidence of interstitial lesions was 71%. Chronic interstitial nephritis was rare in dogs under 1 year old. Glomerulonephritis did not seem to induce interstitial nephritis. Glomerulonephritis occurred not only in kidneys with severe interstitial damage, but also in those with slight damage. The indicated that glomerulonephritis occurred independently of interstitial nephritis. In end-stage kidneys with severe fibrosis, mesangial changes seemed to predominate.

Age Factors↗

PubMed1979

Dysplasia of the kidneys, liver, and pancreas: report of a variant of Ivemark's syndrome.

A newborn girl with respiratory distress due to bilateral pneumothorax was found to be anuric, and died at 18 hours of age. Autopsy revealed a large pancreatic cyst, multiple large hepatic cysts, congenital hepatic fibrosis, bilateral dysplastic kidneys, and dysplasia of the pancreas. These findings constitute a variant of Ivemark's syndrome of dysplasia of the pancreas, liver, and kidneys.

Brain↗

PubMed1979

Carcinogenicity of chloroform.

Chloroform is carcinogenic in rats, mice, and probably in dogs. Chloroform induced carcinomas of the liver and kidney and malignant tumors in other organs in rats and mice. Liver neoplasms have been described in three strains of mice. Carcinomas of the kidney were found in a first study in mice and in the repeat of that study. Dogs given chloroform developed neoplasms of the liver as well as in other organs. Rats given chloroform also developed toxic changes, particularly male rats, as a result of treatment. These lesions included interstitial fibrosis of the kidney; polyarteritis of the mesenteric, pancreatic, and other arterioles and arteries; and atrophy of the testes. These toxic changes may have interfered with the development of neoplasms in male rats.

Adenoma, Bile Duct↗

PubMed1979

Mycotoxicosis produced in swine by cultural products of an isolate of Aspergillus ochraceus. I. Clinical observations and pathology.

Pigs fed a ration, 25% of which was rice culture, of Aspergillus ochraceus lost weight or failed to gain and became depressed. Some pigs died and most developed subcutaneous edema, hydrothorax, hydroperitoneum, pulmonary atelectasis, edema of the mesentery and perirenal edema. Microscopic lesions in addition to edema were primarily renal and consisted of tubular degeneration and necrosis, hyaline tubular casts, interstitial fibrosis and tubular cell regeneration. The first change found after 3 days was cytoplasmic vacuolation of the convoluted and straight segments of the proximal tubules. Necrotic proximal tubules were found after 4 days and after 9 days degeneration and necrosis involved predominantly proximal tubular segments. Pigs fed a ration, 12.5% of which was rice culture, for 8 weeks did not develop perirenal edema but had firm kidneys. Extensive interstitial fibrosis of the cortical labyrinth was the principal change. Within the fibrous connective tissue, some tubules were necrotic and others were atrophied.

Animals↗

PubMed1979

Carcinogenicity of endrin.

Endrin is carcinogenic for rats, and most likely also for mice and dogs. Endrin caused significant incidences of malignant neoplasms at all sites. In one study, female rats were susceptible to the development of neoplasms of the endocrine organs, particularly carcinomas of the adrenal and pituitary glands as well as neoplasms of the reproductive system. In other studies, female rats tended to have carcinomas of the endocrine system, the mammary gland and reproductive system, and male and female rats lymphomas. Rats developed unusual malignant neoplasms, such as Kupffer cell sarcomas of the liver and sarcomas of the mammary gland, uterus, and stomach. There also were toxic changes, particularly in male rats, ingesting endrin. These lesions included interstitial fibrosis of the kidney; polyarteritis of the mesenteric, pancreatic and other arteries; and atrophy of the testes. Such lesions generally interfere with the health of the rats and with the development of neoplasms. Dog receiving endrin for two years had bone marrow hyperplasia, lesions of the thyroid gland and lesions of the skeletal muscle, and hyperplasias or neoplasms of other organs. One female dog had an early carcinoma of the thyroid gland. Mice ingesting endrin developed increased incidences of carcinomas of the liver and sarcomas of the uterus.

Adenoma↗

PubMed1979

Abnormalities of the vas deferens and epididymis in cryptorchid boys with congenital rubella.

Cryptorchidism was present in 12% of 316 boys with congenital rubella (CR) followed by The Roosevelt Hospital Rubella Project. Eight of these patients, age 4 through 16 yr, had a recent orchiopexy, 4 on the left, 2 on the right, and 2 bilaterally. The vasoepididymal system was absent or apparently obstructed in 60% of the 10 sides. The epididymis was abnormal in 6 instances and the vas deferens in 5. Sixty-one boys of the entire series had an intravenous pyelogram (IVP) that was significantly abnormal in 18%. The 8 patients described all had a normal IVP except for 2 who had a malrotated kidney on the involved side. In 5 of the 8, a known maternal rubella infection has occurred during the first 8 wk of gestation. As the rubella virus is known to interfere with cellular growth and tissue differentiation in early pregnancy, it apparently altered the developing testis and mesonephric duct system. Similar vasoepididymal abnormalities have been described previously in patients with uncomplicated cryptorchidism, inguinal hernia, kidney defects, cystic fibrosis and male sterility. Their presence should alert the clinician to perform an IVP and also consider a diagnosis of congenital rubella.

Adolescent↗

PubMedDate not supplied

Carcinogenicity of kepone.

Five studies of the carcinogenicity of the chlorinated pesticide Kepone (chlordecone) in animals were reviewed. Examination of histological sections showed that Kepone is unmistakably carcinogenic in rats and mice. Kepone induced malignant tumors in the liver of rats and mice in the National Cancer Institute studies and in the liver in rats in the Medical College of Virginia study. Malignant tumors were also found in organs other than the liver rats, including those on the lowest dose, in both studies. Female rats given Kepone were more likely to develop malignant tumors than male rats. There also were toxic changes, particularly in male rats. These included interstitial fibrosis of the kidney; polyarteritis of the mesenteric, pancreatic, and other arteries; and atrophy of the testes. Such lesions generally interfere with the health of the rats and with the development of tumors. Atrophy of the testes also prevents reproduction.

Animals↗

PubMed1979

Carcinogenicity of toxaphene: a review.

Toxaphene is highly carcinogenic in rats and mice. Toxaphene induced malignant neoplasms of the liver in rats. Neoplasms at all sites, as well as malignant neoplasms, were increased in male and female rats ingesting toxaphene. Sarcomas were found more often in male rats and carcinomas in female rats. Neoplasms of the endocrine organs were also increased in male and female toxaphene-treated rats. The incidence of neoplasms of the reproductive system was increased in female rats, as was the incidence of mammary gland neoplasms in male rats. Toxic changes in male rats given toxaphene included interstitial fibrosis of the kidney and atrophy of the testes. Toxaphene induced malignant neoplasms of the liver in male and female mice. The incidence of malignant neoplasms at all sites was also increased. In addition to hepatic neoplasms, male mice had leukemia or lymphosarcoma and females had sarcomas of the uterus.

Adrenal Gland Neoplasms↗

PubMed1979

[Kidney polycystic disease as the major feature in three adults with congenital hepatic fibrosis. 3 cases (author's transl)].

Congenital hepatic fibrosis is nearly always associated with ectasia of collecting tubules of the kidneys. This abnormality usually remains silent. In this study we report three cases of adult's CHF with associated renal failure treated by hemodialysis. In all three cases, renal injuries were indistinguishable from those found in adult-type of polycystic disease. The kidneys of our third patient, who underwent two nephrectomies at a 14-years interval, showed ectasia of the collecting tubules with only a few cortical cysts. The second one showed numerous large cysts and only a few ectatic tubules. Our data indicate that: renal failure can complicate the CHF course in adults. Uremia can be the pressenting feature; polycystic kidneys in CHF are microscopically different from those found in adult-type, they might be considered as the final stage in ectasia of collecting tubules.

Adult↗

PubMed2024

The secreted micropeptide C4orf48 enhances renal fibrosis via an RNA-binding mechanism.

Renal interstitial fibrosis is an important mechanism in the progression of chronic kidney disease (CKD) to end-stage kidney disease. However, we lack specific treatments to slow or halt renal fibrosis. Ribosome profiling identified upregulation of a secreted micropeptide, C4orf48 (Cf48), in mouse diabetic nephropathy. Cf48 RNA and protein levels were upregulated in tubular epithelial cells in human and experimental CKD. Serum Cf48 levels were increased in human CKD and correlated with loss of kidney function, increasing CKD stage, and the degree of active interstitial fibrosis. Cf48 overexpression in mice accelerated renal fibrosis, while Cf48 gene deletion or knockdown by antisense oligonucleotides significantly reduced renal fibrosis in CKD models. In vitro, recombinant Cf48 (rCf48) enhanced TGF-β1-induced fibrotic responses in renal fibroblasts and epithelial cells independently of Smad3 phosphorylation. Cellular uptake of Cf48 and its profibrotic response in fibroblasts operated via the transferrin receptor. RNA immunoprecipitation-sequencing identified Cf48 binding to mRNA of genes involved in the fibrotic response, including Serpine1, Acta2, Ccn2, and Col4a1. rCf48 binds to the 3'UTR of Serpine1 and increases mRNA half-life. We identify the secreted Cf48 micropeptide as a potential enhancer of renal fibrosis that operates as an RNA-binding peptide to promote the production of extracellular matrix.

Animals↗

PubMed1979

Liver abnormalities in three patients with fetal alcohol syndrome.

Liver abnormalities were found in three patients with fetal alcohol syndrome. The histological appearance was different in each case. Thick, sclerotic central veins were seen in two of the three cases. One patient had features typical of congenital hepatic fibrosis and cystic disease of the kidneys. Findings in these patients indicate that some cases of congenital hepatic fibrosis might be caused by high maternal alcohol ingestion in pregnancy.

Adolescent↗

PubMed2026

Small-Molecule Degradation of the MicroRNA-21 Precursor Rescues Pathogenic Pathways in Cellular Models of Fibrosis.

MicroRNAs (miRNAs) are short RNA molecules that bind to target mRNAs, resulting in translational repression and gene silencing. Overexpression of microRNA-21 (miR-21) is associated with various human diseases, including autosomal dominant polycystic kidney disease (ADPKD) and pulmonary fibrosis. In this study, a previously described heterobifunctional molecule, TGP-21-RiboTAC, that degrades the miR-21 precursor (pre-miR-21) in triple-negative breast cancer cells was investigated in polycystic kidney cell lines and a lung fibroblast cell line. In the former, TGP-21-RiboTAC degraded pre-miR-21 and derepressed miR-21's downstream targets, programmed cell death 4 (PDCD4) and peroxisome proliferator-activated receptor alpha (PPARα), known drivers of ADPKD. The heterobifunctional molecule also inhibited cyst growth and rescued the metabolic alterations that occur in ADPKD. In the lung fibroblast cell line, MRC-5, TGP-21-RiboTAC also reduced pre- and mature miR-21 levels, rescued transforming growth factor β (TGF-β)-induced repression of SMAD family member 7 (SMAD7), and inhibited cell invasion. Collectively, these studies demonstrate the potential of targeted RNA degradation as therapeutic agents that retard the development of organ fibrosis.

MicroRNAs↗

PubMed1978

The pathology and pathogenesis of chronic lead nephropathy occurring in Queensland.

Many children who suffered acute lead poisoning in Queensland eventually died with contracted kidneys. In most cases the kidneys were granular and showed microscopically fibrosis, hypertensive vascular changes and "alterative glomerulitis". Clinically in these patients, hypertension and chronic renal insufficiency had always preceded death which was usually due to uraemia. In a minority of cases the kidneys showed the changes of benign hypertension but were unusually small; fibrosis and "alterative glomerulitis" were not present. Clinically these patients had had hypertension but minimal renal insufficiency and death was usually due to cerebral haemorrhage. The evidence indicates that lead caused severe damage to the kidney at the time of the lead intoxication by some mechanism other than hypertension. The sequence of events postulated comprises severe renal damage with destruction of glomeruli during childhood lead poisoning, disappearance of the destroyed tissue during childhood and adolescence, onset of hypertension in adolescence or early adult life, gradual onset and progress of chronic uraemia during which fibrosis and granularity developed. In milder cases the sequence is not complete because renal function has remained adequate.

Adult↗