Biomedical subjects

C C Nast

Publications and source records attributed to C C Nast.

At least 37 records · Page 2Linked to original sources

PubMed1997

Parvovirus B19 infection-related complications in renal transplant recipients: treatment with intravenous immunoglobulin.

BACKGROUND: Chronic red cell aplasia can develop in immunocompromised patients including transplant recipients infected with parvovirus B19 (PV B19). Renal involvement with PV B19 infection is not well-recognized. METHODS: We diagnosed erythroid hypoplasia associated with PV B19 infection in three renal transplant recipients; one of them developed de novo collapsing glomerulopathy. These patients were treated with intravenous immunoglobulin (IVIG). RESULTS: In two patients, anemia responded promptly to IVIG therapy. One of them had recurrence of anemia that responded to a second course of IVIG. Despite IVIG treatment, persistent infection with PV B19, recurrent anemia, and de novo collapsing glomerulopathy leading to allograft failure developed in the third patient, who had received the most intense immunosuppression. CONCLUSIONS: These findings indicate that PV B19 infection in transplant recipients can cause chronic red cell aplasia that generally responds to IVIG therapy. In some patients, particularly those who are heavily immunosuppressed, infection may persist despite treatment. As the cellular receptor for PV B19 is expressed in the kidney, persistent infection may result in development of glomerulopathies in these patients.

Adult↗

PubMed1997

Long-term allograft acceptance in a patient with posttransplant lymphoproliferative disorder: correlation with intragraft viral interleukin-10.

BACKGROUND: Viral (v) interleukin (IL)-10 is expressed by Epstein-Barr virus (EBV) and has pro- and anti-inflammatory actions similar to human IL-10. EBV is also a known factor in the development of posttransplant lymphoproliferative disorder (PTLPD) in allograft recipients. We observed a patient with widespread PTLPD 9 months after renal transplantation, who subsequently maintained renal function despite minimal immunosuppression, and we investigated a possible link between these factors. METHODS: The patient's chart was reviewed for relevant history. EBV DNA in blood and tissues was assessed by polymerase chain reaction. Human and vIL-10 and gamma-interferon mRNA were evaluated with reverse transcription-polymerase chain reaction using nested primers. RESULTS: After the diagnosis of PTLPD, the patient was maintained on prednisone (8 mg/day) as the only immunosuppression with preserved renal function for 17 months until death as a result of pulmonary failure. She had continuously high blood levels of EBV DNA, although only mild persistent intrarenal atypical lymphocytic infiltrates. Human IL-10 mRNA was never present; in contrast, intragraft vIL-10 mRNA was identified and associated with resolution of an intervening episode of severe acute transplant rejection. CONCLUSIONS: We suggest that the preserved renal function resulted from the anti-inflammatory actions of vIL-10 inhibiting acute rejection in the renal allograft.

Adult↗

PubMed1997

Ureteritis and cholecystitis: two unusual manifestations of cytomegalovirus disease in renal transplant recipients.

BACKGROUND: Common clinical manifestations of cytomegalovirus (CMV) infection include flu-like symptoms with fever, diarrhea, leukopenia, and elevated liver enzymes. Diagnosis is made by detection of the virus by buffy-coat blood culture or by polymerase chain reaction (PCR) analysis. METHODS: Here we describe two renal transplant recipients who presented with unusual manifestations of CMV disease (cholecystitis and ureteritis). In both patients, no symptoms or signs of systemic CMV infection were present, and they were thought to have other common causes for cholecystitis and ureteral obstruction. RESULTS: Retrospective analysis of peripheral blood by PCR analysis was positive for CMV DNA. Histologic examination of the resected gall bladder and stenotic ureteric segment showed CMV inclusions, confirmed subsequently by in situ hybridization. Thus, we report that CMV infection may present with acute cholecystitis or ureteral obstruction without its classical clinical symptoms. CONCLUSIONS: Because CMV infection is common in transplant patients, the atypical manifestations of CMV should be considered in the differential diagnosis of posttransplant complications. Detection of CMV DNA in the peripheral blood by PCR analysis may help identify these patients.

Adult↗

PubMed1997

Voriconazole (UK-109,496) inhibits the growth and alters the morphology of fluconazole-susceptible and -resistant Candida species.

The effects of voriconazole on the growth, ultrastructure, and leakage of cytoplasmic materials of Candida species were investigated. MIC data showed that voriconazole was more active than fluconazole. Exposure of yeast to voriconazole caused growth inhibition, cell wall thinning, and cell membrane degradation. Neither cell collapse nor release of cytoplasmic materials was observed in the treated cells.

Antifungal Agents↗

PubMed1997

The cytoplasmic membrane is a primary target for the staphylocidal action of thrombin-induced platelet microbicidal protein.

Thrombin-induced platelet microbicidal protein (tPMP-1) is a small, cationic peptide released from rabbit platelets exposed to thrombin in vitro. tPMP-1 is microbicidal against a broad spectrum of bloodstream pathogens, including Staphylococcus aureus. Preliminary evidence suggests that tPMP-1 targets and disrupts the staphylococcal cytoplasmic membrane. However, it is not clear if the cytoplasmic membrane is a direct or indirect target of tPMP-1. Therefore, we assessed the in vitro activity of tPMP-1 versus protoplasts prepared from logarithmic-phase (LOG) or stationary-phase (STAT) cells of the genetically related S. aureus strains 19S and 19R (tPMP-1 susceptible and resistant, respectively). Protoplasts exposed to tPMP-1 (2 microg/ml) for 2 h at 37 degrees C were monitored for lysis (decrease in optical density at 420 nm) and ultrastructural alterations (by transmission electron microscopy [TEM]). Exposure to tPMP-1 resulted in substantial lysis of LOG but not STAT protoplasts of 19S, coinciding with protoplast membrane disruption observed by TEM. Thus, it appears that tPMP-1-induced membrane damage is influenced by the bacterial growth phase but is independent of the staphylococcal cell wall. In contrast to 19S, neither LOG nor STAT protoplasts of 19R were lysed by tPMP-1. tPMP-1-induced membrane damage was further characterized with anionic planar lipid bilayers subjected to various trans-negative voltages. tPMP-1 increased conductance across bilayers at -90 mV but not at -30 mV. Once initiated, a reduction in voltage from -90 to -30 mV diminished conductance magnitude but did not eliminate tPMP-1-mediated membrane permeabilization. Therefore, tPMP-1 appears to directly target the staphylococcal cytoplasmic membrane as a primary event in its mechanism of action. Specifically, tPMP-1 likely leads to staphylococcal death, at least in part by permeabilizing the bacterial membrane in a voltage-dependent manner.

Animals↗

PubMed1997

Evaluation of pathologic criteria for acute renal allograft rejection: reproducibility, sensitivity, and clinical correlation.

This study was designed to evaluate the pathologic criteria used for acute renal allograft rejection that were developed by a panel of renal pathologists participating in the Cooperative Clinical Trials in Transplantation, a National Institutes of Health-supported, multicenter research group. The panel defined three categories of acute rejection. (1) Type I: mononuclear infiltrate in > or =5% of cortex, a total of at least three tubules with tubulitis in 10 consecutive high-power fields from the most severely affected areas, and at least two of the three following features: edema, activated lymphocytes, or tubular injury. (2) Type II: arterial, or arteriolar, endothelialitis with or without the preceding features. (3) Type III: arterial fibrinoid necrosis or transmural inflammation with or without thrombosis, parenchymal necrosis, or hemorrhage. Using these criteria, and without any knowledge of the clinical course or original diagnosis, a rotating panel of three pathologists agreed with the original study pathologist's diagnosis of the presence or absence of rejection in 259 of the 286 biopsies (91%) used for this analysis (kappa = 0.80). The sensitivity to establish the diagnosis of rejection was 91% for a single core and 99% for two cores. To validate the diagnostic criteria, the thresholds for number of tubules with tubulitis and the percent infiltrate were varied, and the pathologic diagnosis was compared with the clinical course. The greatest agreement occurred with a threshold of > or =1 tubule with tubulitis and > or =5% cortex with interstitial infiltrate (91%). Clinically severe rejection episodes were correlated with the type of rejection (type I, odds ratio [OR] 6.2; type II, OR 37.9). Type II rejection was more likely to be clinically severe than type I (OR 6.1). Analysis of other individual pathologic features revealed a correlation with clinical severity for endothelialitis (OR 13.2), interstitial hemorrhage (OR 13.2), and the presence of glomerulitis (OR 3.7) (all P < 0.05). The extent of tubulitis or of the interstitial infiltrate did not correlate with severity (P > 0.05). It is concluded that these criteria are simple, reproducible, and clinically relevant. These data should lead to further refinement of the diagnostic systems for renal allograft rejection.

Acute Disease↗

PubMed1997

The effect of transfection of antisense cDNA for procollagen alpha 1 (IV) on stimulated proliferation in rat glomerular endothelial cells.

Glomerular endothelial cells were stably transfected with a pMAMneo-Blue vector recombinant for procollagen alpha 1 (IV) cDNA in the sense (S) or antisense (AS) orientation utilizing a calcium phosphate precipitation technique. Cellular clones resistant to G418 antibiotic were selected and expanded for further analysis. Immunofluorescence microscopy demonstrated less Type IV collagen in the AS clones (1.0 +/- 0.3) than in control parent (P) and S clones (2.0 +/- 0.4) (P < 0.05). Western analysis showed that the AS clones synthesized 20 +/- 10% of the 205-kd alpha 1 (IV) chain of Type IV collagen compared with P cells (P < 0.05). As transfected clones demonstrated similar basal proliferation rates as control cells when cultured in 0.5% fetal calf serum (FCS), but failed to undergo fetal calf serum (FCS)-stimulated hyperplasia when grown on standard fibronectin-coated surfaces in 40% FCS (P < 0.05, compared with P- and S-transfected control cells). There were significant linear relationships between the presence of Type IV collagen as detected by either immunofluorescence microscopy or alpha 1 (IV) peptide chain quantitation by Western analysis and the ability of cells to undergo FCS-stimulated hyperplasia when grown on fibronectin (P < 0.05). Growth on a surface comprised of fibronectin plus Type IV collagen restored the capacity of AS transfected cells to respond to FCS stimulation (P < 0.001), but had no significant effect on the proliferative behavior of P or S cells. Measurements of AS RNA levels in these cells suggest that the inhibition of stimulated proliferation is determined by the presence of a threshold quantity of cellular AS RNA. These data demonstrate that Type IV collagen plays a critical role in conditioning glomerular endothelial cells to respond to proliferative stimuli.

Animals↗

PubMed1996

Expression of transforming growth factor-beta isoforms in human glomerular diseases.

Protein and mRNA expression of TGF-beta isoforms, TGF-beta 1, -beta 2 and -beta 3, and deposition of fibronectin containing extra domain A (fibronectin EDA+) and plasminogen activator inhibitor-1 (PAI-1) were studied in human chronic glomerulonephritis and diabetic nephropathy. Normal kidneys showed similar, weak immunostaining for all three TGF-beta isoforms. TGF-beta mRNA expression was weak for all isoforms with TGF-beta 1 > TGF-beta 3 >> TGF-beta 2. In thin basement membrane disease and minimal change disease, disorders where extracellular matrix accumulation is not a feature, immunoreactivity and mRNA expression did not differ from normal. In contrast, diseases characterized by extracellular matrix accumulation (IgA nephropathy, focal and segmental glomerulosclerosis, crescentic glomerulonephritis, lupus nephritis and diabetic nephropathy) all showed significantly increased expression of the three TGF-beta isoforms in glomeruli and the tubulointerstitium. While glomerular and tubulointerstitial deposition of two matrix components induced by TGF-beta, fibronectin EDA+ and PAI-1, was significantly elevated in all diseases with matrix accumulation, correlation analysis revealed a close relationship primarily with TGF-beta 1. We conclude that, for a spectrum of human glomerular disorders, increased protein expression of all three TGF-beta isoforms and proteins induced by TGF-beta is associated with pathological accumulation of extracellular matrix.

Antibody Specificity↗

PubMed1995

Interleukin-12 mRNA levels in renal allograft fine-needle aspirates do not correlate with acute transplant rejection.

TH1 cytokines, including gamma-interferon (IFN), are critical in the initiation and progression of allograft rejection. As interleukin (IL)-12 up-regulates gamma-IFN, we assessed the role of IL-12 in human transplant rejection. Twenty renal allograft fine-needle aspirates from 19 patients were obtained, evaluated in the standard fashion, and assessed for gamma-IFN and IL-12p40 subunit mRNA levels using nested reverse transcriptase polymerase chain reaction. Ten aspirates demonstrated acute rejection by clinical criteria, and 9 of the 10 aspirates contained gamma-IFN while only 3 demonstrated IL-12; there were no distinguishing characteristics for these 3 patients with regard to therapy, or time of onset and severity of rejection. Seven patients without clinical or morphologic rejection failed to demonstrate gamma-IFN or IL-12. Three patients had discrepant findings; there was no morphologic rejection, yet all 3 patients contained gamma-IFN and 1 patient demonstrated rejection on subsequent biopsy. However, only 1 aspirate exhibited IL-12 and this patient had no documented subsequent rejection. This study confirms the association of gamma-IFN mRNA with acute rejection. In contrast, IL-12 mRNA does not appear to play a key role early in the rejection process.

Acute Disease↗

PubMed1995

Renal transplant fine needle aspiration and cytokine gene expression.

Fine needle aspiration of renal transplants is a safe effective means of obtaining intragraft material for diagnostic evaluation of transplant dysfunction in the first 3-6 months post engraftment. Aspiration can be performed daily as an outpatient to assess causes of renal insufficiency and response to therapeutic intervention. Aspiration also provides a unique tool for the investigation of pathogenetic mechanisms in acute rejection; samples can be subjected to reverse transcriptase-polymerase chain reaction with quantitation of cytokine gene expression. We have utilized this technique to demonstrate the strong, likely causal, relationship between gamma-interferon and acute rejection. The ability to perform aspirates frequently affords an opportunity to map the cytokine cascade prior to and during episodes of acute rejection. This may identify new areas for therapeutic intervention during the process of rejection.

Biopsy, Needle↗

PubMed1995

Up-regulation of transforming growth factor alpha binding sites in experimental rabbit colitis.

BACKGROUND & AIMS: Transforming growth factor alpha (TGF-alpha), a member of the epidermal growth factor family, has been proposed to mediate protection against mucosal injury and promote healing of the gastrointestinal mucosa. TGF-alpha acts via a plasma membrane receptor, which is distributed throughout the digestive system with the highest density in epithelia. The aim of this study was to investigate the pattern of TGF-alpha binding sites in the normal and inflamed rabbit colon. METHODS: The immune complex/formalin model of acute colitis and tissue section receptor autoradiography were used. Inflammation was characterized by cellular infiltration, edema, and necrosis. TGF-alpha binding relative density was determined by densitometry on film autoradiograms. RESULTS: The normal colon had a low to moderate density of specific TGF-alpha binding sites in the mucosa and external muscle. TGF-alpha binding density was significantly increased in the mucosa at 4 hours and remained higher than normal for up to 48 hours. The density of binding sites in the mucosa and the inflammatory index returned to near normal values at 96 hours, when colitis had subsided. CONCLUSIONS: The increase in TGF-alpha binding in the mucosa during experimental colitis supports the hypothesis that members of the epidermal growth factor family play a role in inflammation, perhaps acting as mediators of mucosal protection and repair.

Acute Disease↗

PubMed1995

Anti-inflammatory effects of CGP 47969A, a novel inhibitor of proinflammatory cytokine synthesis, in rabbit immune colitis.

BACKGROUND & AIMS: Proinflammatory cytokines such as interleukin (IL) 1, IL-8, and tumor necrosis factor (TNF) have been implicated as primary mediators of intestinal inflammation. The aim of the present study was to determine the effects of a novel cytokine antagonist (CGP 47969A) in a rabbit model of acute colitis. METHODS: Colitis was induced using the formalin-immune complex technique. Animals were pretreated intrarectally with CGP 47969A (30, 10, or 3 mg/kg), hydrocortisone (0.8 mg/kg), or vehicle (4 mL saline) 2 hours before the induction of colitis and twice daily thereafter until death 48 hours after the induction of colitis. The severity of inflammation of colonic tissue was assessed using histological analysis and myeloperoxidase activity assay, and IL-1 alpha, IL-8, TNF-alpha, and IL-1 receptor antagonist levels were determined. RESULTS: Compared with vehicle, CGP 47969A (10 mg/kg) significantly reduced the acute inflammatory index by 58%, edema by 67%, necrosis by 99%, and myeloperoxidase activity by 49% (all P < 0.02) with efficacy similar to that of steroids. These effects were associated with a significant inhibition of colonic IL-1 alpha and IL-8 by 56% and 90%, respectively (p < 0.01). CONCLUSIONS: Administration of CGP 47969A reduces inflammation and tissue damage in rabbit immune complex colitis through mechanisms involving the inhibition of mucosal proinflammatory cytokines.

Animals↗

PubMed1995

Intrarenal extramedullary erythropoiesis in renal allograft fine-needle aspirates.

Recombinant human erythropoietin (rhEPO) is widely used in patients with end-stage renal disease and occasionally in renal allograft recipients to correct anemia. Red blood cell production is markedly increased by rhEPO; however, no extramedullary erythropoiesis (EME) has been associated with this hormone. We observed intrarenal EME in five allograft fine-needle aspirates performed for reduced graft function in four patients between 3.7 and 7 weeks following transplantation. These four patients received rhEPO during dialysis and three resumed rhEPO therapy after transplantation; all four remained anemic. Donors were between 13 months and 13 years of age, with one pediatric and three adult recipients. Aspirates with apparently incidental EME contained all stages of red blood cell precursors, but these cells were not observed in corresponding peripheral blood samples. The hematopoietic cells could be readily distinguished from cells of lymphoid origin. There were no correlations between intragraft EME and aspirate or clinical diagnosis referable to renal dysfunction. Aspirates performed prior to 3.7 weeks or after 7 weeks did not demonstrate EME. These data suggest that endogenous EPO and rhEPO in anemic patients receiving pediatric renal allografts may activate red blood cell precursors in the young graft, inducing intrarenal EME. Recognition of this entity is important to distinguish it from immune activation or malignancy within the donor organ.

Adult↗

PubMed1995

Prevention of experimental cyclosporin-induced interstitial fibrosis by losartan and enalapril.

The pathogenesis of renal scarring in chronic cyclosporin nephropathy is unknown. In this study, we evaluated the effects of renin-angiotensin system blockade by enalapril and losartan in a salt-dependent model of cyclosporin-associated chronic tubulointerstitial fibrosis (TIF). Rats kept on normal or low-salt diet were given cyclosporin, cyclosporin+enalapril, cyclosporin+losartan, cyclosporin+enalapril#losartan, or vehicle for 14 and 28 days. Cyclosporin reduced glomerular filtration rate (GFR) in rats fed either diet, but only salt-depleted animals developed significant TIF. Cyclosporin also impaired renal concentrating ability and caused tubular enzymuria. Renin-angiotensin system blockade decreased blood pressure (BP) and promoted afferent arteriolar vasodilatation. Losartan reduced plasma renin activity and prevented cyclosporin-induced increment of cortical alpha 1(I) procollagen mRNA. Renin-angiotensin blockade did not improve GFR and tubular function; however, it strikingly prevented TIF development, even in presence of very low BP. Rats treated with cyclosporin, hydralazine, and furosemide achieved BP values similar to losartan or enalapril groups, but there was no protection against interstitial fibrosis development. These results suggest that cyclosporin-related chronic interstitial injury is mediated by angiotensin II and that the mechanisms promoting the interstitial scarring can be dissociated from glomerular and tubular dysfunction in cyclosporin nephropathy.

Animals↗

PubMed1995

Transforming growth factor-beta and matrix protein expression in acute and chronic rejection of human renal allografts.

Because the increased tissue expression of TGF-beta underlies fibrosis in many diseases, it was hypothesized that sustained elevated transforming growth factor (TGF)-beta overexpression might be responsible for fibrosis in chronic rejection of the renal allograft. To test this hypothesis, biopsies were obtained from 5 patients with acute rejection, 5 patients with chronic rejection, 10 normal individuals, and 10 patients with kidney disease. The tissues were examined by immunofluorescence for the three TGF-beta isoforms (1, 2, and 3) and the two matrix proteins induced by TGF-beta that serve as markers of fibrosis: fibronectin extradomain A positive (EDA+) and plasminogen activator inhibitor-1 (PAI-1). The tubulointerstitium from all cases of acute rejection and chronic rejection showed highly significant increases in immunostaining for the three TGF-beta isoforms (P < 0.001), fibronectin EDA+ (P < 0.005), and PAI-1 (P < 0.001). In the glomeruli, only TGF-beta 1 expression achieved statistical significance (P < 0.005) in acute rejection, whereas in chronic rejection, all three TGF-beta isoforms (p < 0.001) in addition to fibronectin EDA+ (p < 0.001) and PAI-1 (p < 0.001) were elevated. There was both cellular and matrix staining of the TGF-beta isoforms. In striking contrast, control kidney tissues were negative or only weakly positive. Because TGF-beta was present both in acute and in chronic rejection but not in control tissues and because acute rejection episodes are a good predictor for chronic rejection, these results suggest that TGF-beta may play a role in the pathogenesis of fibrosis in chronic rejection.

Acute Disease↗

PubMed1994

Gamma-interferon gene expression in human renal allograft fine-needle aspirates.

Cytokines appear to play a major role in acute transplant rejection (AR); however, the specific cytokines initiating AR are not known. To investigate gamma-interferon messenger RNA (mRNA) as a key factor in AR induction, we performed reverse transcription-polymerase chain reaction (RT-PCR) on renal allograft fine-needle aspirates (FNA). Fifteen FNA from 15 patients were processed and interpreted in the standard fashion, the percent of tubular cells with MHC class II expression (DR) quantitated, and aliquots of FNA obtained for RT-PCR. RT-PCR was performed with primers to gamma-IFN with cyclophylin and insulin primers as controls. Retrospective clinical diagnoses were made for each FNA sample. Following RT-PCR, all FNA and FNAs from control normal and AR nephrectomy specimens had cyclophylin present, and in the 9 samples tested insulin was absent. Five patients had AR clinically and by FNA criteria; all 5 had elevated DR and gamma-IFN mRNA present in FNA. Five patients had tubular necrosis or cyclosporine toxicity clinically, and FNA without immune activation or elevated DR and negative gamma-IFN mRNA. Two patients had immune activation by FNA with elevated DR; both FNA expressed gamma-IFN mRNA by Southern blot, one only weakly, and both patients subsequently developed clinical AR. Two patients had recently treated AR, one with persistent DR elevation without-immune activation and negative gamma-IFN mRNA in FNAs. This study demonstrates that RT-PCR can be performed with renal allograft FNA samples. The findings suggest intragraft gamma-IFN mRNA expression occurs in active AR preceding clinical AR, thus defining incipient AR. Detection of gamma-IFN mRNA may offer an early diagnostic tool for detection of AR.

Base Sequence↗

PubMed1994

Neutralization of endogenous IL-1 receptor antagonist exacerbates and prolongs inflammation in rabbit immune colitis.

Administration of exogenous interleukin-1 receptor antagonist (IL-1ra) is effective in reducing the severity of disease in animal models of acute inflammation. However, the function of endogenous IL-1ra in this process, is not yet known. We investigated the pathophysiological role of IL-1ra in a rabbit model of formalin-immune complex colitis. This model has previously been shown to be IL-1 mediated and a reduction in disease severity is observed with exogenous IL-1ra treatment. Colonic IL-1ra was found to be elevated subsequent to IL-1, and exceeded IL-1 levels 10-fold. Peak levels of IL-1ra preceded both the resolution of colitis and a significant decrease in IL-1 production. Administration of specific neutralizing antibodies against rabbit IL-1ra increased mortality and prolonged intestinal inflammatory responses. A significant increase in IL-1 alpha colonic tissue levels was also measured as a result of exogenous anti-IL-1ra treatment. These studies are the first demonstration that endogenous IL-1ra may play an important role in regulating the host's inflammatory response by counteracting the deleterious and possibly lethal effects of IL-1 produced during acute inflammation.

Animals↗

PubMed1993

Identification of tubular cell nephron segment origin in renal fine-needle aspirates.

Currently there are no definitive criteria for identification of the nephron segment origin of tubular cells in renal fine-needle aspirates. This information would be useful for determining the cortical or medullary location of aspirate specimens. To establish morphologic criteria for identifying tubular cell origin, we evaluated 60 allograft and four native kidney aspirates with immunocytochemistry (IC) and May-Grünwald-Giemsa (MGG) stains. IC markers included URO-3 and Tetragonolobus purpuras for proximal cells, URO-5 and Arachis hypogaea for distal cells, and URO-5, Arachis hypogaea, and anti-cytokeratin antibody for collecting duct cells. Cell and nuclear areas were measured morphometrically, and cell grouping and MGG staining characteristics were assessed. Proximal tubular cells have an area of 335 +/- 112 microns2 (IC strains) and 350 +/- 107 microns2 (MGG stain) with a nuclear:cytoplasm (N:C) ratio of 1:4. The cells occur singly or in small clusters of four to seven cells with abundant pale cytoplasm. Distal tubular cells measure 224 +/- 66 microns2 (IC stains) and 171 +/- 38 microns2 (MGG stain) with an N:C ratio of 1:2. They often form honeycomb aggregates of 10 to 20 cells with moderately dense cytoplasm. Cells of collecting ducts have areas of 96 +/- 32 microns2 (IC stains) and 99 +/- 35 microns2 (MGG stain) with an N:C ratio of 2:3. These cells are found in glandular clusters of two to seven cells with dense cytoplasm. All tubular cell size and staining characteristics were the same in allograft and native kidney samples.(ABSTRACT TRUNCATED AT 250 WORDS)

Biopsy, Needle↗