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PubMed1996

Glycosylation of the Na+/H+ exchanger isoform NHE-3 is species specific.

The glycosylation of Na+/H+ exchanger isoform NHE-3 was studied in brush border membrane (BBM) vesicles isolated from rabbit, dog, and rat kidney cortex. Western blot analyses were performed against BBM proteins by using polyclonal antibodies to an NHE-3 fusion protein. In rabbit kidney, NHE-3 antibody recognized a band with approximately 95 kd molecular mass. Treatment of rabbit cortical BBM with glycopeptidase F, at 16 U/ml, for 4 or 16 hours increased the apparent mobility of NHE-3 to 84 and 82 kd, respectively. Incubation of rabbit BBM proteins for 16 hours with endoglycosidase H, at 0.1 U/ml, did not alter the apparent mobility of NHE-3. Deglycosylation of NHE-3 with glycopeptidase F did not affect acid-stimulated, amiloride-sensitive sodium 22 influx in BBM vesicles as compared with that in controls (p > 0.05). Immunoblot analysis against BBM proteins from canine kidney cortex demonstrated the presence of an approximately 83 to 92 kd protein. Treatment of canine BBM with glycopeptidase F or endoglycosidase H or F for 16 hours did not alter the apparent mobility of NHE-3, suggesting that canine renal NHE-3 is not glycosylated. Treatment of canine kidney BBM with glycopeptidase F did not affect acid-stimulated 22Na+ influx as compared with that in controls (p > 0.05). Immunoblot analysis against BBM proteins from rat kidney cortex demonstrated the presence of a sharp band at 90 kd. Treatment of rat BBM with glycopeptidase F or endoglycosidase H or F for 16 hours did not alter the apparent mobility of NHE-3, suggesting that rat renal NHE-3 is not glycosylated. The above experiments suggest that NHE-3 glycosylation in mammalians is species specific and that glycosylation does not affect the exchanger activity.

Animals↗
PubMed1996

rK7-kallikrein in rat kidney and urine.

Rat Kidney is reported to contain the rK7-kallikrein gene expressed at a high mRNA level. However, there is no direct evidence that the rK7 enzyme is present in kidney or urine. We have analyzed rat kidney and urine for rK7-like enzyme activity, using distinctive properties of purified rK7 enzyme (hydrolysis of specific substrate, inhibition by SBTI). Rat urine and kidney cortex contain substantial levels of rK7-like enzyme activity. Nearly 40% of the enzyme in urine is in an active form while nearly all of the rK7 in kidney cortex is in the inactive form. Treatment with low salt diet and mineralocorticoid increases rK7 in both kidney cortex and urine approximately 2-fold. The percentage of active enzyme in urine increases markedly on this regimen.

Animals↗
PubMed1982

Inhibition of kidney lysosomal phospholipases A and C by aminoglycoside antibiotics: possible mechanism of aminoglycoside toxicity.

Nephrotoxicity is an important side effect of aminoglycoside antibiotics, which are used to control infections caused by Gram-negative bacteria. Accumulation of aminoglycosides and phospholipids in the lysosomes is a prominent and early feature of aminoglycoside nephrotoxicity and is characterized histologically by the presence of numerous multilamellar bodies in kidney proximal tubule cells. Previous studies have shown that the drug-induced phospholipid fatty liver in man and animals is due to concentration of certain cationic amphiphilic drugs in lysosomes with inhibition of lysosomal phospholipases. It seemed possible that this mechanism might also explain the elevated levels of phospholipid and increased numbers of multilamellar bodies reported in the kidney cortex in aminoglycoside nephrotoxicity. In this study, subcellular localization of acid phospholipases A and C has been shown to be lysosomal in rat kidney cortex. A soluble lysosomal protein fraction was isolated and found to contain both phospholipase A and phospholipase C activity. Streptomycin did not inhibit the release of fatty acids from [3H]dioleoylphosphatidylcholine. However, amikacin, dibekacin, gentamicin, and tobramycin inhibited both phospholipase A and phospholipase C. Our results suggest that the accumulation of phospholipids in lysosomes of kidney cortex, an early and pervasive feature of acute aminoglycoside nephrotoxicity, is due to inhibition of lysosomal phospholipases.

Aminoglycosides↗
PubMed2002

Epithelial COX-2 expression is not regulated by nitric oxide in rodent renal cortex.

In the adult rodent kidney cortex, cyclooxygenase-2 (COX-2), NO synthase (NOS1), and renin synthesis change in parallel on alterations in distal tubular NaCl concentration, and their products in part may mutually determine synthesis and activity of these enzymes. Epithelial NO synthesis has been postulated to exert a stimulatory role on COX-2 expression. Changes in COX-2 and NOS1 may be assessed histochemically by determining changes in the number of positive cells. In rat, macula densa and adjacent cells may co-express COX-2 and NOS1, whereas cell groups of the upstream thick ascending limb (cTAL) express COX-2 alone. We have tested whether the stimulation of COX-2 expression by short- and long-term unilateral renal artery stenosis, low salt, and furosemide treatment depends on co-expression of NOS1. These conditions produced significant respective increases (40% to 351%, P<0.05) in the number of COX-2 immunoreactive cells, regardless of whether NOS1 was present or not, suggesting that co-expression of NOS1 is not necessary to produce these changes. Under high-salt conditions, analogous though inverse changes were recorded (-62% to -73%, P<0.05). In mice with genetic deletion of NOS1, low- and high-salt diets caused similar changes of COX-2 immunoreactivity (106% and -52%, P<0.05) than those seen in wild-type mice (43% and -78%, P<0.05). We conclude that alterations of distal tubular NaCl concentration and presumably NaCl transport induce changes in epithelial COX-2 expression that does not depend on presence of co-expressed NOS1. It therefore seems unlikely that NO is part of a signal transduction chain between tubular chloride sensing and the modulating effects of prostaglandins in tubulo-vascular information transfer.

Animals↗
PubMed1998

Detection and quantitation of a sodium-dependent sulfate cotransporter (NaSi-1) by sandwich-type enzyme-linked immunosorbent assay.

The sodium-dependent sulfate transporter (NaSi-1) DNA has been recently identified from rat kidney cortex. The objective of this study was to develop a quantitative assay for the NaSi-1 transporter protein. The NaSi-1 antigen was prepared by fusion protein techniques following analysis of the primary sequence for antigenicity. Polyclonal and monoclonal antibodies against the NaSi-1 antigen were raised in rabbits and mice, respectively. The specificity of the raised antibodies was examined by Western analysis using brush-border membrane (BBM) and basolateral membrane (BLM) purified from rat kidney cortex. Both NaSi-1 polyclonal and monoclonal antibodies detected a 69-kDa protein in the BBM. Using the purified monoclonal antibody as the capture antibody and the polyclonal antibody as the detecting antibody, a simple and sensitive sandwich-type enzyme-linked immunosorbent assay was developed to quantitate NaSi-1 transporter protein levels in tissue. The specificity of the assay was examined using BBM, BLM and NaSi-1-transfected Madin-Darby canine kidney cells. The assay was capable of detecting NaSi-1 at levels as low as 6.58 fmol. The concentration of NaSi-1 transporter protein in crude membrane isolated from rat kidney cortex was 0.094+/-0.014 fmol/ microg protein (mean+/-SD of three preparations).

Animals↗
PubMed1992

Occurrence of alpha 1-2-fucosylation in membrane glycoproteins of Morris hepatoma 7777 but not in liver. Aberrant type of fucosylation in a malignant tissue.

A comparative study was undertaken to characterize the linkages of L-fucose in N-glycans of plasma membrane glycoproteins from Morris hepatoma 7777, host liver and kidney cortex, as well as from rat serum. After in-vivo radiolabelling of rats with L-[6-3H]fucose, the asparagine-linked carbohydrate chains were released from delipidated plasma membrane glycoproteins, as well as from serum glycoproteins, by enzymic digestion with peptide-N4-(N-acetyl-beta-glucosaminyl)asparagine amidase from Flavobacterium meningosepticum. They were then converted to their corresponding oligosaccharide alditols by reduction with sodium borohydride. Two specific alpha-L-fucosidases from almond emulsin and from Aspergillus niger, combined with affinity HPLC on immobilized Aleuria aurantia lectin were used to study the linkage of L-fucose in the oligosaccharide chains. Fucose alpha 1-2 linked to galactose, was present only in the plasma membrane of hepatoma 7777 (18% of total L-[3H]fucose in N-glycans), but was not expressed in host liver, kidney cortex and serum. None of the investigated sources contained an appreciable amount of fucose alpha 1-3/4 linked to N-acetyl-D-glucosamine. All the radioactively labelled oligosaccharides from host liver, kidney cortex and serum, but only 82% of these oligosaccharides from hepatoma, contained alpha-fucosyl residues linked at the C6 position of the proximal N-acetyl-D-glucosamine.

Animals↗
PubMed1996

Nonpeptide angiotensin II receptor antagonists: in vivo inhibition of [125I-Sar1,Ile8]angiotensin II binding by losartan, EXP597 and L-159,282 in rats.

Effects of losartan, L-159,282 and EXP597 on the in vivo binding of [125I-Sar1,Ile8]angiotensin II to kidney cortex and adrenal were examined in rats. Losartan, an AT1 receptor antagonist, completely blocked [125I-Sar1,Ile8]angiotensin II binding to the kidney cortex which contains only AT1 binding sites with an ID50 of 0.06 mg/kg. Losartan partially inhibited [125I-Sar1,Ile8]angiotensin II binding to the adrenal which contains equal amounts of AT1 and AT2 binding sites. Blockade by the AT1 receptor antagonist L-159,282 sufficiently increased the plasma levels of angiotensin II to block the AT2 receptor. EXP597 inhibited [125I-Sar1,Ile8]angiotensin II binding to the kidney cortex and adrenal almost totally with ID50s of 0.05 and 0.06 mg/kg, respectively. This result suggests that EXP597 exhibits almost equal binding affinity for AT1 and AT2 binding sites in vivo in rats.

Angiotensin II↗
PubMed2006

Different isoform patterns for vascular endothelial growth factor between clear cell and papillary renal cell carcinoma.

OBJECTIVE: To investigate the protein expression of vascular endothelial growth factor (VEGF) isoforms in relation to the clinical course in patients with different renal cell carcinoma (RCC) types, as angiogenesis is essential for tumour growth and metastasis. PATIENTS AND METHODS: Western blots were assayed of protein extracts from tumour and concomitant kidney cortex samples from 96 patients. The levels of VEGF189, VEGF165, and VEGF121 isoforms were correlated with clinicopathological characteristics and survival. RESULTS: VEGF189 levels were significantly higher in kidney cortex and chromophobe RCC than in papillary and conventional RCC. In papillary RCCs, VEGF189 levels correlated inversely with tumour stage and tumour size. VEGF165 levels were higher in kidney cortex than in RCC, but there was no difference among the RCC types. VEGF121 expression was associated with less advanced tumour stage in conventional RCC. Using multivariate analysis, VEGF189 remained as an independent prognostic factor for patients with papillary RCC. CONCLUSIONS: VEGF189 was associated with tumour progression; in papillary RCC, VEGF189 was a significant independent prognostic factor. VEGF protein isoform patterns differed among the specific RCC types. Additional knowledge is essential to design new anti-angiogenic therapies for all RCC types.

Adult↗
PubMed1983

Detection of a nafenopin-binding protein in rat liver cytosol associated with the induction of peroxisome proliferation by hypolipidemic compounds.

[3H]nafenopin, a known inducer of liver peroxisomal enzymes, was shown to bind to a specific, saturable pool of binding sites in cytosols from rat liver and kidney cortex. Tissue levels of this binding protein (liver greater than kidney cortex; not detectable in myocardium, skeletal muscle) were seen to correlate with the ability of nafenopin to induce peroxisomal enzymes in these organs. Clofibrate and ciprofibrate, which are structurally similar to nafenopin, competitively blocked the specific binding of [3H]nafenopin. Phenobarbital, a non-inducer of peroxisomes, and [4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio]acetic acid and 4-chloro-6-(2,3-xylidino)-2-pyrimidinylthio(N-beta-hydroxyethyl)acetamide, which are structurally unrelated peroxisome proliferators, did not complete for the specific [3H]nafenopin binding sites. The [3H]nafenopin binding protein is proposed as a mediator of the drug-induced increase in peroxisomes and associated peroxisomal enzymes.

Animals↗
PubMed1993

In vitro characterization of estrogen induced Syrian hamster renal tumors: comparison with an immortalized cell line derived from diethylstilbestrol-treated adult hamster kidney.

Primary diethylstilbestrol-induced kidney tumors from Syrian hamsters were grown in vitro and maintained in culture for 6 mo. Combined immunohistochemical studies using antibodies to intermediate filaments and ultrastructural studies of tumor cells in culture exhibited characteristics similar to tumor cells in vivo. Furthermore, the cells manifested transformed properties in culture; they grew both as multilayered colonies attached to the tissue culture substrate and as floating multicellular colonies (spheroids). When cultured cells were injected into diethylstilbestrol-treated recipient hamsters, tumors developed at the injection sites. In contrast, renal tubules or whole kidney cortex from control hamsters cultured in the same medium underwent only short-term growth, with senescence developing after approximately 1 mo. However, cell cultures of kidney cortex from animals treated in vivo for 5 mo. with diethylstilbestrol formed a cell line. This diethylstilbestrol-induced cell line has been maintained in culture for 1.5 yr and has the following characteristics: a) it is anchorage-dependent, b) it is negative in in vivo tumorigenicity tests, and c) cultured cells are histochemically and ultrastructurally similar to cultured tumor cells. This culture system should prove to be of use in studying hormonal carcinogenesis in vitro.

Animals↗
PubMed2002

Down-regulation of rat organic cation transporter rOCT2 by 5/6 nephrectomy.

BACKGROUND: In rat kidneys, the organic ion transporters rOCT1, rOCT2, rOAT1 and rOAT3 are considered to mediate the basolateral uptake of various ionic compounds. However, their changes in chronic renal failure (CRF) are poorly understood. The present study examined the renal handling of organic ions and the expression of these transporters under CRF. METHODS: 5/6 Nephrectomized rats were used as the animal model of CRF. Renal handlings of cimetidine and paraaminohippuric acid (PAH) were examined by in vivo experiments. rOAT1, rOAT3, rOCT1 and rOCT2 expressions were determined by Western blotting. RESULTS: The tubular secretion rates of both PAH and cimetidine were markedly decreased in CRF rats. Although the distribution rates of PAH into the kidney cortex and medulla, and of cimetidine into the kidney cortex were maintained, the distribution rate of cimetidine into the kidney medulla was significantly decreased in CRF rats. The expression level of the rOCT2 protein was markedly depressed in CRF rats, but those of rOCT1, rOAT1 and rOAT3 were maintained. In addition, the plasma concentration of testosterone, a regulator of rOCT2 expression, was significantly reduced by CRF. Both the renal clearance of cimetidine and rOCT2 expression were recovered by the exogenous administration of testosterone in CRF rats. CONCLUSIONS: The levels of urinary excretion of cationic drugs, especially substrates for rOCT2, were reduced under CRF partly due to the reduced expression of rOCT2, and the lowered plasma level of testosterone was suggested to be responsible for the depressed rOCT2 expression in CRF.

Animals↗
PubMed1992

Identification of endothelin receptor subtypes in human renal cortex and medulla using subtype-selective ligands.

High affinity and high density endothelin (ET)-binding sites were identified in membranes prepared from human kidney cortex and medulla. Saturation binding experiments performed in membranes prepared from cortex and medulla using [125I]ET-1 and [125I]ET-3 revealed that the proportion of [125I]ET-3-binding sites was 30-35% less than that of [125I]ET-1-binding sites. The apparent dissociation constants and maximum binding for [125I]ET-1 and [125I]ET-3 to membranes from cortex were 91 +/- 5 pM and 165 +/- 10 fmol/mg protein, and 117 +/- 9 pM and 110 +/- 7 fmol/mg protein, respectively, whereas in medulla they were 139 +/- 10 pM and 360 +/- 11 fmol/mg protein, and 142 +/- 11 pM and 245 +/- 15 fmol/mg protein, respectively. In the presence of 10 nM sarafotoxin-6c, which is selective for ETB receptors, [125I]ET-1 binding was decreased by 65-70%, whereas [125I]ET-3 binding was totally abolished, suggesting that 65-70% of [125I]ET-1 binding and 100% of [125I]ET-3 binding was to ETB receptors. This was further confirmed by the use of a cyclic pentapeptide [cyclo(D-Trp,D-Asp,L-Pro, D-Val,L-Leu)] (BQ123), which is selective for ETA receptors. In the presence of 1 microM BQ123, [125I]ET-1 binding was decreased by 25-30%, whereas [125I]ET-3 binding was unaffected, confirming that 30-35% of ET receptors belong to the ETA subtypes, and that [125I]ET-1 bound to both ETA and ETB receptors with the same high affinity, but [125I]ET-3 bound only to ETB receptors with high affinity. These results suggest that human kidney cortex and medulla contain ETA and ETB receptors in a ratio of 30:70, and that sarafotoxin-6c and BQ123 are valuable tools in identifying the subtype of ET receptors in various tissues.

Cell Membrane↗
PubMed2006

Free-ranging European bisons accumulate more cadmium in the liver and kidneys than domestic cattle in north-eastern Poland.

It has been shown that free-ranging big game animals accumulate several-fold more cadmium (Cd) in the liver and kidneys than domestic animals. To examine possible reasons for this difference, in the present work we determined the concentrations of Cd in the liver and kidney cortex of European bisons (n=23) from Białowieza Forest (north-eastern Poland) and domestic cattle (n=15) from the same region; in addition, analyses of Cd in the grasses and soil as well as of soil pH were carried out. The accumulation of Cd in liver and kidney cortex of the female bisons correlated significantly with the age up to 7 years, but stabilized thereafter. The 7-12-year-old bisons had 2.14- and 2.25-fold higher concentrations of Cd in the liver and kidney cortex, respectively, than the age-matched domestic cattle. Notably, the Cd levels in the liver and kidneys of the 8-12-year-old cattle were comparable to those found in the 2-year-old and 4-6-year-old bisons, respectively. The content of Cd in the grasses from Białowieza Forest appeared to be 2.1-fold higher than that in the plants from the pastures. Similarly, the concentration of water-extractable Cd in the soil was 2.7-fold greater in Białowieza Forest than in the pastures, despite the fact that nitric acid-extractable Cd (total Cd) was similar in the soils from the two sites. The concentration of water-extractable Cd in the soil as well as the content of Cd in the grasses inversely correlated with soil pH, which appeared to be significantly lower in Białowieza Forest. These data indicate that soil pH is probably responsible for the higher concentrations of Cd in the feed and tissues of bisons as compared with those of domestic cattle.

Animals↗
PubMed1979

Neoplastic transformation-linked alterations in arginyl-tRNA synthetase activity.

The behavior of the activity of arginyl-tRNA synthetase (L-arginine : tRNAArg Ligase(AMP-forming), EC 6.1.1.19) was determined in extracts of rat liver: normal adult, normal proliferating (from developing and from partially hepatectomized rats), and neoplastic (hepatomas of different growth rates) and in extracts of rat kidney cortex and transplantable kidney tumors. The Km values for arginine, ATP, and tRNA of the enzyme of the rapidly growing hepatoma 3924A were the same as those of the enzyme from the liver of control rats. The pH optima of the control and neoplastic livers were in the same range of 7.25-8.0. Taking the hepatic specific activity for arginyl-tRNA synthetase as 100%, deep layer of gut, thymus and testis had higher activity; renal cortex and spleen had the same activity; and skeletal muscle, brain, heart, lung, superficial layer of gut and adipose tissue had lower activity. In a wide spectrum of hepatomas of different growth rates, a significant increase of 1.4-2.4-fold in arginyl-tRNA synthetase activity was observed when compared with that of liver of control normal rats. This elevation in enzyme activity in hepatomas appears to be specific to neoplasia, since it is unaltered in regenerating and low in differentiating liver. The increase in arginyl-tRNA synthetase in the liver tumors appears to be transformation-linked, since the activity was increased in all hepatomas, even in the slowest growing ones. Furthermore, the increase in enzyme activity was not limited to hepatic neoplasms, since a rise was also observed in transplantable rat kidney tumors. Thus, the reprogramming of gene expression in neoplastic tissue entails an increase in arginine-tRNA synthetase activity.

Aging↗
PubMed1986

[Occurrence of phenylalanine hydroxylase in the human kidney].

Phenylalanine hydroxylase activity, determined by fluorimetric procedure in human kidney (cortex) of 17 patients, who had a kidney operation, was on the average 4.7 nkat tyr/g protein (25 degrees C), which is 28% in comparison to the enzyme activity in human liver. This is in good accordance with the results of AYLING et al. who investigated 15 human kidneys. They found by the spectrophotometric method 22% of the liver enzyme activity. A nonspecific hydroxylation could be excluded by tests with the inhibitors p-Cl-phenylalanine, 3-I-tyrosine and 6-F-tryptophan.

Adult↗
PubMed1994

Proliferation of human renal cell carcinoma studied with in vivo iododeoxyuridine labelling and immunohistochemistry.

Tumor cell proliferation is one interesting cell biological parameter of possible predictive value for prognosis. In the present study 176 tumor and 33 kidney cortex samples from 33 patients with renal cell carcinoma were studied after immunohistochemical detection of in vivo labelled iododeoxyuridine. The tumors had a mean labelling index (LI) of 1.06 +/- 0.59%, significantly different from LI of kidney cortex tissue 0.08 +/- 0.09% (p < 0.001). There was a tendency towards increasing LIs at higher clinical stages. No correlation was found between LI and tumor size. A significant difference existed for LIs between diploid and aneuploid tumors (p = 0.037). Within the limited number of patients with a relatively short follow-up, Kaplan-Meier curves indicated that LI might provide prognostic information.

Adult↗
PubMed2000

Content of non-mercury-associated selenium in human tissues.

Recent studies have shown that at a higher mercury (Hg) burden, the molar ratio of selenium (Se) and Hg in tissues tends to approximate 1:1 by the formation of biologically largely inert adducts. From the toxicological standpoint, this trapping of free Hg is welcome. However, this binding of Se to Hg reduces the portion of Se in tissues, which is available for the formation of essential selenoenzymes like glutathione peroxidase, type I deiodase, and so forth and could result in a relative deficiency of Se. Therefore, we tried to determine the concentration of non-Hg-associated Se in several human tissues. As there is no proved trace method for the speciation of non-Hg-bound and Hg-bound Se in tissues, the total concentrations of Hg and Se were determined and the portion of non-Hg-associated Se was calculated by the difference of the molar concentrations of Se and Hg. For this investigation, the following tissues were obtained by autopsy from 133 adults: kidney cortex, thyroid gland, liver, spleen, cerebrum cortex, and pituitary gland. In no case was an occupational Hg burden known. The results confirm the assumption of a 1:1 association of Hg and Se in human tissues. The mean concentration of non-Hg-bound Se was calculated to 576 microg/kg in the kidney cortex, 363 microg/kg in the thyroid gland, 308 microg/kg in the liver, 205 microg/kg in the spleen, 111 microg/kg in the cerebrum cortex, and 545 microg/kg in the pituitary gland. In none of the cases under investigation in any tissue was the molar Se/Hg ratio below 1. This means that a total deficiency of non-Hg-bound Se could not be seen in this normal population, even at a higher Hg burden. Nevertheless, at a suboptimal Se supply like in Germany, any reduction of the part of Se, which is available for the formation of essential seleno-enzymes, should be avoided. Therefore, any additional Hg burden such as from dental amalgam should to be considered critically. The different distribution of Hg and Se in the body confirms that there is a controlled hierarchy in the Se supply of different organs, which tries to prevent a Se deficiency in organs with essential seleno-enzymes like the thyroid gland even under an suboptimal Se supply.

Adolescent↗
PubMed1992

A high-affinity folate binding protein in proximal tubule cells of human kidney.

High-affinity 3H-folate binding in solubilized brush border membranes of human kidney cortex display characteristics such as apparent positive cooperativity typical of specific folate binding. The folate binding activity and the activity of the brush border membrane-marker enzyme, gamma-glutamyltransferase, were eightfold higher in brush border membranes compared to crude kidney homogenate. Ultrogel AcA 44 chromatography revealed a major (Mr approximately 100 kDa) and a minor (Mr approximately 25 kDa) folate binding protein in brush border membranes. The large molecular size form may represent a membrane-derived hydrophobic folate binding protein inserted in Triton X-100 micelles. This notion was supported by the identical molecular weights of the 100 kDa and 25 kDa folate binding peaks determined by sodium dodecylsulfate polyacrylamide gel electrophoresis and immunoblotting. The folate binding protein in renal brush border membranes cross reacted with rabbit antibodies against 25 kDa human milk folate binding protein, and showed immunoprecipitation in the presence of these antibodies. Paraffin embedded sections of kidney cortex showed immunostaining of cells in the convoluted proximal tubules after exposure to rabbit antiserum (1:8000 dilution). Glomeruli and distal tubules showed no immunostaining.

Carrier Proteins↗