Nephrosis
Puromycin Aminonucleoside
Nephrosis, Lipoid
Nephrotic Syndrome
Kidney Glomerulus
Hemoglobinuria
Puromycin
Carboprost
Podocytes
Puromycin aminonucleoside nephrosis results in a marked increase in fractional clearance of albumin. (1/199)
Puromycin aminonucleoside nephrosis (PAN) results in a marked increase in the fractional clearance of albumin. The increase in the fractional clearance of [(3)H]albumin to approximately 0.045, as measured both in vivo and in the isolated perfused rat kidney (IPK) with PAN, occurs without an accompanying equivalent increase in glomerular capillary wall size selectivity as previously measured with dextrans. This is very similar to the marked increase in albuminuria seen with kidneys treated with inhibitors of endocytosis by the tubular epithelium, particularly lysine (T. M. Osicka, L. M. Pratt, and W. D. Comper. Nephrology 2: 199-212, 1996). The similarity is further established that, like in the presence of lysine, [(3)H]albumin excreted in urine from rats with PAN is essentially intact whereas, in both in vivo and IPK control experiments, excreted [(3)H]albumin is heavily degraded. The same observations have also been made for (3)H-labeled anionic horseradish peroxidase. These observations suggest that the significant albuminuria that occurs in PAN is primarily post-glomerular basement membrane in origin. (+info)Inhibition of nuclear factor-kappaB activation reduces cortical tubulointerstitial injury in proteinuric rats. (2/199)
BACKGROUND: Protein-induced chemokine expression in proximal tubular cells is mediated by the transcription factor nuclear factor-kappa B (NF-kappaB). We hypothesized that in vivo inhibition of renal NF-kappaB activation would reduce interstitial monocyte infiltration in a rat model of nonimmune proteinuric tubulointerstitial inflammation. METHODS: Male Wistar rats received a single intravenous injection of doxorubicin hydrochloride [adriamycin (ADR), 7.5 mg/kg] and were studied 7, 14, 21, and 28 days later. In a second study, inhibitors of NF-kappaB [N-acetylcysteine (NAC; 150 mg/kg, b.i.d., i.p.), pyrrolidine dithiocarbamate (PDTC, 50 mg/kg, b. i.d., i.p.)] or vehicle were commenced on day 14 after the onset of proteinuria and were continued until day 30. RESULTS: Rats injected with ADR had increased proteinuria (UpV, day 28, 474 +/- 57; control, 18 +/- 2 mg/day; P < 0.01) and cortical tubulointerstitial injury [tubule cell atrophy, interstitial volume, and monocyte/macrophage (ED-1) infiltration]. Electrophoretic mobility shift assay of nuclear extracts from whole cortex of ADR rats demonstrated that NF-kappaB activation (p50/65, p50/c-Rel) increased from day 7 (4.7 +/- 0.2 fold-increase above control; P < 0.01) was maximal at day 28 (6.2 +/- 0.7; P < 0.01) and correlated with UpV (r = 0.63; P < 0.05) and interstitial ED-1 infiltration (r = 0.67; P < 0.01). Chronic treatment of ADR rats with PDTC suppressed NF-kappaB activation (by 73%; P < 0.05) without any effect on UpV. NF-kappaB inhibition with PDTC was accompanied by a reduction in tubule cell atrophy (59%; P < 0.01), interstitial volume (49%; P < 0.05) and ED-1 infiltration (48%; P < 0.01), and cortical lipid peroxidation (41%; P < 0.05) compared with vehicle-treated ADR rats. In contrast NAC had no effect on NF-kappaB activation, tubulointerstitial injury, or UpV in ADR rats. CONCLUSION: The activation of NF-kappaB may have an important role in mediating cortical interstitial monocyte infiltration and tubular injury in nonimmune proteinuric tubulointerstitial inflammation. (+info)Mortality from nephritis and nephrosis in the fibreglass manufacturing industry. (3/199)
OBJECTIVES: To investigate the question of whether there is an association between exposure to silica or respirable glass fibre and mortality from nephritis or nephrosis among workers in fibrous glass wool manufacturing facilities. METHODS: A case-control study with cases and controls derived from the Owens Corning mortality surveillance system. Two case-control analyses were carried out, one where the cases are defined with nephritis or nephrosis as the underlying cause of death and one where cases are defined as those where nephritis or nephrosis is either the underlying or a contributing cause of death. RESULTS: There is no consistent relation between respirable fibres or respirable silica and nephritis or nephrosis when the analysis is based either on underlying cause only or on underlying plus contributing cause of death. None of the sociodemographic variables considered suggests an increased risk when considering both underlying and contributing cause of death. CONCLUSIONS: These data would seem to support the contention that the most accurate picture of renal disease will be gained from the use of all information on the death certificate and not only the underlying cause. For these data, all odds ratios (ORs) for respirable fibres and silica based on both underlying and contributing cause of death are < 1 with the exception of the highest exposure to silica which is slightly > 1 (OR = 1.04). Although these results do not prove that there is no association between nephritis and nephrosis and exposure to fibreglass or silica in the fibreglass manufacturing environment, they do not support the assertion that such an association exists. (+info)Cloning and expression of the rat nephrin homolog. (4/199)
Despite of the increased availability of genetically modified mouse strains, the experimental models in the rat have provided the most widely employed and versatile models for the study of renal pathophysiology and functional genetics. The identification of the human gene mutated in the congenital nephrotic syndrome of the Finnish type (NPHS1) has recently been reported, and its protein product has been termed nephrin. Here we report the molecular cloning and characterization of rat nephrin cDNA. Rat nephrin cDNA has an open reading frame of 3705 bp, shows 82% sequence identity with human nephrin cDNA, and shows characteristic rat-specific splicing variants. The translated nucleotide sequence has 89% sequence identity at the amino acid level. The signal sequence, glycosylation, and cysteine localization patterns are nearly identical to those of human nephrin. As in the human, the rat nephrin transcript is expressed in a tissue-restricted pattern. Antipeptide antibodies raised to the intracellular nephrin-specific domain identified immunoreactivity exclusively within the rat kidney glomerulus by indirect immunofluorescence. Initial results with semiquantitative reverse transcriptase-polymerase chain reaction analysis showed a remarkable down-regulation of nephrin-specific mRNA in the puromycin nephrosis of the rat. (+info)Stress-induced gastric lesion formation is prevented in rats with daunomycin-induced nephrosis. (5/199)
In the present study, we investigated the susceptibility to restraint plus water-immersion stress (RWIS) in rats with daunomycin-induced nephrosis in comparison to that in normal rats. The severity of RWIS-induced gastric lesions was significantly less in nephrotic rats on the 20th and 40th days after a single i.v. injection of daunomycin (12 mg/kg) than in the respective control rats. Acid secretion in pylorus-ligated rats significantly decreased under the 3-h stress. On the 20th day after treatment with daunomycin, acid secretion was significantly less in nephrotic rats than in control rats under both stress and unstressed conditions. Pretreatment of normal rats with methylene blue, a guanylate cyclase inhibitor, or phenylephrine, a vasoconstrictor, significantly prevented the stress-induced gastric lesions and decreased acid secretion. N(omega)-Nitro-L-arginine methyl ester, a nitric oxide (NO) synthase inhibitor, prevented the stress-induced gastric lesion formation only. These results indicate that nephrotic rats are more resistant to RWIS-induced gastric lesions than normal rats. In addition, these results suggest that the decrease in acid secretion related to the decrease in the release of NO from endothelial cells may contribute, at least in part, to the prevention of the stress-induced gastric lesion formation in nephrotic rats. (+info)Reproductive function in male rats with chronic nephrosis. (6/199)
Endocrine dysfunction has been associated with renal diseases. The present study was conducted to explore reproductive function in male rats with chronic nephrosis. Experimental chronic nephrosis was induced by the administration of 7.5, 5.0 and 5.0 mg per 100 g body weight of puromycin aminonucleoside on days 0, 21 and 35, respectively. Reproductive function was evaluated on the basis of hormonal concentrations, mass of accessory sex organs and fertility during an 84 day period. Circulating LH, FSH, testosterone and oestradiol concentrations were measured by specific radioimmunoassays, while fertility was estimated by the rate of pregnancy induction. Samples were collected on days 7, 14, 28, 56 and 84. The results showed an important endocrine dysfunction characterized by low concentrations of LH and FSH during the first month, after which concentrations were similar to control values or even increased on days 56 and 84. Testosterone and oestradiol decreased significantly at all time points evaluated. The mass of the testes did not alter. However, the mass of the prostate and seminal vesicle decreased only during the first 2 weeks, and became essentially normal thereafter. The reproductive capacity of nephrotic males was eliminated on day 7, whereas on day 14, 16% of the group was able to mate successfully and subsequently most animals recovered their normal reproductive function. This study demonstrates for the first time that rats with experimental chronic nephrosis develop an important endocrine dysfunction, characterized mainly by persistent reduction in testosterone concentrations, which impairs reproductive capacity only transiently. (+info)Mercury induces regional and cell-specific stress protein expression in rat kidney. (7/199)
Cells respond to physiologic stress by enhancing the expression of specific stress proteins. Heat-shock proteins (hsps) and glucose-regulated proteins (grps) are members of a large superfamily of proteins collectively referred to as stress proteins. This particular stress-protein response has evolved as a cellular strategy to protect, repair, and chaperone other essential cellular proteins. The objective of this study was to evaluate the differential expression of four hsps in the renal cortex and medulla during experimental nephrotoxic injury using HgCl2. Male Sprague-Dawley rats received single injections of HgCl2 (0.25, 0.5, or 1 mg Hg/kg, i.v.). At 4, 8, 16, or 24 h after exposure, kidneys were removed and processed for histopathologic, immunoblot, and immunohistochemical analyses. Nephrosis was characterized as minimal or mild (cytoplasmic condensation, tubular epithelial degeneration, single cell necrosis) at the lower exposures, and progressed to moderate or severe (nuclear pyknosis, necrotic foci, sloughing of the epithelial casts into tubular lumens) at the highest exposures. Western blots of renal proteins were probed with monoclonal antibodies specific for 4 hsps. In whole kidney, Hg(II) induced a time- and dose-related accumulation of hsp72 and grp94. Accumulation of hsp72 was predominantly localized in the cortex and not medulla, while grp94 accumulated primarily in the medulla but not cortex. The high, constitutive expression of hsp73 did not change as a result of Hg(II) exposure, and it was equally localized in cortex and medulla. Hsp90 was not detected in kidneys of control or Hg-treated rats. Since hsp72 has been shown involved in cellular repair and recovery, and since Hg(II) damage occurs primarily in cortex, we investigated the cell-specific expression of this hsp. Hsp72 accumulated primarily in undamaged distal convoluted tubule epithelia, with less accumulation in undamaged proximal convoluted-tubule epithelia. These results demonstrate that expression of specific stress proteins in rat kidney exhibits regional heterogeneity in response to Hg(II) exposure, and a positive correlation exists between accumulation of some stress proteins and acute renal cell injury. While the role of accumulation of hsps and other stress proteins in vivo prior to or concurrent with nephrotoxicity remains to be completely understood, these stress proteins may be part of a cellular defense response to nephrotoxicants. Conversely, renal tubular epithelial cells that do not or are unable to express stress proteins, such as hsp72, may be more susceptible to nephrotoxicity. (+info)Chronic angiotensin II infusion but not bradykinin blockade abolishes the antiproteinuric response to angiotensin-converting enzyme inhibition in established adriamycin nephrosis. (8/199)
Angiotensin-converting enzyme (ACE) inhibition reduces proteinuria in established adriamycin nephrosis. To investigate whether the reduction in proteinuria is due to decreased generation of angiotensin II (AngII) or to decreased degradation of bradykinin, four series of experiments in established adriamycin nephrosis were performed. In the first series, 2 mg/kg lisinopril reduced BP from 117 +/- 4 to 67 +/- 2 mmHg and proteinuria from 335 +/- 66 to 57 +/- 10 mg/24 h after 2 wk of treatment. Subsequent continuous intraperitoneal infusion of AngII (250 ng/kg per min) for 2 wk partially restored proteinuria to 180 +/- 42 mg/24 h, whereas BP increased to 97 +/- 3 mmHg. Subsequent withdrawal of AngII restored the antiproteinuric effects of lisinopril, whereas subsequent withdrawal of lisinopril restored proteinuria to pretreatment values. In the second series, AT1 receptor blockade induced a fall in BP and proteinuria similar to that by lisinopril. In the third series, lisinopril reduced BP from 121 +/- 5 to 68 +/- 2 mmHg and proteinuria from 355 +/- 90 to 101 +/- 10 mg/24 h. Subsequent intraperitoneal infusion of bradykinin antagonist (HOE 140; 1 mg/kg per 24 h) for 2 wk did not affect BP (72 +/- 2 mmHg) or proteinuria (92 +/- 15 mg/24 h). In the fourth series, bradykinin (3 mg/kg per 24 h) was infused for 2 wk to mimic decreased bradykinin breakdown. This did not affect proteinuria, but induced a fall in BP from 114 +/- 3 to 93 +/- 4 mmHg. The BP-lowering effect of exogenous bradykinin was completely reversed by 1 wk infusion of HOE 140 (93 +/- 4 to 113 +/- 4 mmHg), while proteinuria remained unchanged. In conclusion, the antiproteinuric effect of ACE inhibition appears to be independent of bradykinin in this model, supporting a main role for reduction of AngII in the antiproteinuric action of ACE inhibition. (+info)Nephrosis is an older term that was used to describe a group of kidney diseases, primarily characterized by the damage and loss of function in the glomeruli - the tiny filtering units within the kidneys. This results in the leakage of large amounts of protein (primarily albumin) into the urine, a condition known as proteinuria.
The term "nephrosis" was often used interchangeably with "minimal change nephropathy," which is a specific type of kidney disorder that demonstrates little to no changes in the glomeruli under a microscope, despite significant protein leakage. However, current medical terminology and classifications prefer the use of more precise terms to describe various kidney diseases, such as minimal change disease, focal segmental glomerulosclerosis, or membranous nephropathy, among others.
It is important to consult with a healthcare professional or refer to updated medical resources for accurate and current information regarding kidney diseases and their specific diagnoses.
Puromycin aminonucleoside is not a medical condition, but rather a laboratory reagent used in research. It is a synthetic antibiotic and analogue of the amino acid tyrosine, which specifically inhibits protein synthesis in eukaryotic cells by interacting with the peptidyl transferase center of the 60S ribosomal subunit. This compound has been widely used as a tool to study various cellular processes, including programmed cell death (apoptosis), autophagy, and lysosome biogenesis. Prolonged exposure to puromycin aminonucleoside can induce cytopathic effects, such as vacuolization and detachment of cells, which are often used as markers for its effectiveness in inhibiting protein synthesis.
Lipoid nephrosis is a historical term for a kidney disorder now more commonly referred to as minimal change disease (MCD). It is a type of glomerulonephritis which is characterized by the loss of proteins in the urine (proteinuria) due to damage to the glomeruli, the tiny filtering units within the kidneys.
The term "lipoid" refers to the presence of lipids or fats in the glomeruli, which can be observed under a microscope. However, it's worth noting that not all cases of MCD involve lipid accumulation in the glomeruli.
MCD is typically idiopathic, meaning its cause is unknown, but it can also occur as a secondary condition related to other medical disorders such as allergies, infections, or medications. It primarily affects children, but can also occur in adults. Treatment usually involves corticosteroids and other immunosuppressive therapies to control proteinuria and prevent kidney damage.
Nephrotic syndrome is a group of symptoms that indicate kidney damage, specifically damage to the glomeruli—the tiny blood vessel clusters in the kidneys that filter waste and excess fluids from the blood. The main features of nephrotic syndrome are:
1. Proteinuria (excess protein in urine): Large amounts of a protein called albumin leak into the urine due to damaged glomeruli, which can't properly filter proteins. This leads to low levels of albumin in the blood, causing fluid buildup and swelling.
2. Hypoalbuminemia (low blood albumin levels): As albumin leaks into the urine, the concentration of albumin in the blood decreases, leading to hypoalbuminemia. This can cause edema (swelling), particularly in the legs, ankles, and feet.
3. Edema (fluid retention and swelling): With low levels of albumin in the blood, fluids move into the surrounding tissues, causing swelling or puffiness. The swelling is most noticeable around the eyes, face, hands, feet, and abdomen.
4. Hyperlipidemia (high lipid/cholesterol levels): The kidneys play a role in regulating lipid metabolism. Damage to the glomeruli can lead to increased lipid production and high cholesterol levels in the blood.
Nephrotic syndrome can result from various underlying kidney diseases, such as minimal change disease, membranous nephropathy, or focal segmental glomerulosclerosis. Treatment depends on the underlying cause and may include medications to control inflammation, manage high blood pressure, and reduce proteinuria. In some cases, dietary modifications and lifestyle changes are also recommended.
A kidney glomerulus is a functional unit in the nephron of the kidney. It is a tuft of capillaries enclosed within a structure called Bowman's capsule, which filters waste and excess fluids from the blood. The glomerulus receives blood from an afferent arteriole and drains into an efferent arteriole.
The process of filtration in the glomerulus is called ultrafiltration, where the pressure within the glomerular capillaries drives plasma fluid and small molecules (such as ions, glucose, amino acids, and waste products) through the filtration membrane into the Bowman's space. Larger molecules, like proteins and blood cells, are retained in the blood due to their larger size. The filtrate then continues down the nephron for further processing, eventually forming urine.
Proteinuria is a medical term that refers to the presence of excess proteins, particularly albumin, in the urine. Under normal circumstances, only small amounts of proteins should be found in the urine because the majority of proteins are too large to pass through the glomeruli, which are the filtering units of the kidneys.
However, when the glomeruli become damaged or diseased, they may allow larger molecules such as proteins to leak into the urine. Persistent proteinuria is often a sign of kidney disease and can indicate damage to the glomeruli. It is usually detected through a routine urinalysis and may be confirmed with further testing.
The severity of proteinuria can vary, and it can be a symptom of various underlying conditions such as diabetes, hypertension, glomerulonephritis, and other kidney diseases. Treatment for proteinuria depends on the underlying cause and may include medications to control blood pressure, manage diabetes, or reduce protein loss in the urine.
Hemoglobinuria is a medical condition characterized by the presence of hemoglobin in the urine. Hemoglobin is a protein found in red blood cells that carries oxygen throughout the body. Normally, when red blood cells die, they are broken down and their hemoglobin is recycled. However, in certain conditions such as intravascular hemolysis (the destruction of red blood cells inside blood vessels), hemoglobin can be released into the bloodstream and then filtered by the kidneys into the urine.
Hemoglobinuria can be a symptom of various underlying medical conditions, including hemolytic anemias, disseminated intravascular coagulation (DIC), severe infections, snake bites, and exposure to certain toxins or medications. It is important to identify the underlying cause of hemoglobinuria, as treatment will depend on the specific condition.
In some cases, hemoglobinuria can lead to kidney damage due to the toxic effects of free hemoglobin on the renal tubules. This can result in acute or chronic kidney injury, and in severe cases, it may require dialysis or transplantation.
Puromycin is an antibiotic and antiviral protein synthesis inhibitor. It works by being incorporated into the growing peptide chain during translation, causing premature termination and release of the incomplete polypeptide. This results in the inhibition of protein synthesis and ultimately leads to cell death. In research, puromycin is often used as a selective agent in cell culture to kill cells that have not been transfected with a plasmid containing a resistance gene for puromycin.
Citrinin is a mycotoxin, which is a toxic compound produced by certain types of fungi. It is commonly produced by Penicillium citrinum and Aspergillus terreus. Citrinin has been found to contaminate various food and feed commodities, including cereals, fruits, vegetables, and dairy products.
Clinically, citrinin exposure can cause a range of toxic effects in humans and animals, including nephrotoxicity (kidney damage), hepatotoxicity (liver damage), genotoxicity (damage to DNA), and immunotoxicity (suppression of the immune system). Symptoms of citrinin poisoning may include nausea, vomiting, diarrhea, abdominal pain, increased urination, and kidney failure.
It is important to note that citrinin contamination in food and feed can be minimized through proper storage, handling, and processing practices. Additionally, regulatory limits have been established in many countries to control the levels of citrinin in food and feed.
Carboprost is a synthetic analogue of prostaglandin F2α, which is a naturally occurring hormone-like substance in the body. It is primarily used as a medical treatment to induce labor or to manage postpartum hemorrhage (severe bleeding after childbirth) due to uterine atony (failure of the uterus to contract).
Carboprost works by causing strong contractions of the uterus, which can help to promote labor or reduce excessive bleeding. It is administered intramuscularly (injected into a muscle) and its effects are usually seen within a few minutes after injection. Common side effects include nausea, vomiting, diarrhea, and fever.
It's important to note that Carboprost should only be used under the supervision of a healthcare professional, as it can have serious side effects if not used properly.
Podocytes are specialized cells that make up the visceral epithelial layer of the glomerular basement membrane in the kidney. They have long, interdigitating foot processes that wrap around the capillaries of the glomerulus and play a crucial role in maintaining the filtration barrier of the kidney. The slit diaphragms between the foot processes allow for the passage of small molecules while retaining larger proteins in the bloodstream. Podocytes also contribute to the maintenance and regulation of the glomerular filtration rate, making them essential for normal renal function. Damage or loss of podocytes can lead to proteinuria and kidney disease.
Nephrosis