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Biomedical subjects

M Haas

Publications and source records attributed to M Haas.

At least 127 records · Page 7Linked to original sources
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

A reevaluation of routine electron microscopy in the examination of native renal biopsies.

Electron microscopy is routinely utilized in most centers in the evaluation of native renal biopsies. Several studies, primarily from the 1960s and early 1970s, provide justification for its use. Conducted by Siegel et al. (1), the largest study evaluated 213 consecutive renal biopsies and found that electron microscopy was needed for a correct diagnosis in 11%, as well as for confirmation or additional information in another 36%. However, nearly all of these studies were conducted before the use of immunofluorescence in renal biopsy diagnosis became widespread and before several new glomerular diseases and variants were described. In light of this situation and the expense of the procedure, the routine use of electron microscopy in native renal biopsies also examined by immunofluorescence and routine light microscopy was reevaluated. From January 1996 to June 1996, 288 native renal biopsies were received, and all were evaluated by the same pathologist. Of those, 233 met criteria for inclusion in this study, which were > or = 5 glomeruli for light microscopy, > or = 2 for immunofluorescence, and > or = 1 for electron microscopy, not including globally scarred glomeruli. Light microscopy (hematoxylin and eosin, periodic acid-Schiff stains) and immunofluorescence--for immunoglobulin (Ig) G, IgA, IgM, C3, C1q, fibrinogen; kappa/lambda when needed--were evaluated on each biopsy within 48 h of receipt, and a preliminary diagnosis was recorded if possible. Electron microscopy was then performed, and a final diagnosis was made. In 50 cases (21%), electron microscopy was needed to make the final diagnosis; in two of these cases, the preliminary diagnosis was incorrect, and in 48, a firm preliminary diagnosis could not be made. In the other cases, the preliminary diagnosis was correct, but in 48 (21%), ultrastructural study was felt to provide important confirmatory data, and in eight cases (3%), an additional, unrelated diagnosis was supported by the ultrastructural findings. Diagnoses most frequently requiring electron microscopy included minimal change nephropathy, early diabetic nephropathy, membranous lupus nephritis, membranoproliferative glomerulonephritis, postinfectious glomerulonephritis, thin basement membrane nephropathy (or exclusion of this in cases of otherwise unexplained hematuria), and human immunodeficiency virus-associated nephropathy (or exclusion of it in cases of collapsing glomerulopathy). Common diagnoses usually not requiring electron microscopy included IgA nephropathy, diffuse proliferative lupus nephritis, focal segmental glomerulosclerosis (not collapsing glomerulopathy variant), pauci-immune crescentic glomerulonephritis, acute interstitial nephritis, and amyloid nephropathy. This study confirms that, as was the case 20 to 30 yr ago, electron microscopy provides useful diagnostic information in nearly half of native renal biopsies. If electron microscopy cannot be performed routinely on all such biopsies, it is recommended that tissue for ultrastructural studies be set aside in each case.

Biopsy↗
PubMed1997

Chiropractic radiologists: a survey of chiropractors' attitudes and patterns of use.

OBJECTIVE: To assess the chiropractic use of radiography, referral patterns to both medical and chiropractic radiologists and attitudes toward radiologists. DESIGN: Random sample mail survey. PARTICIPANTS: Practicing U.S. chiropractors. RESULTS: The response rate was 46% (197 of 425). Seventy-four percent of the respondents have radiographic facilities in their offices. Contraindication screen (71%), pathological diagnosis (63%), biomechanics and posture (51%) and medicolegal protection (27%) were considered important reasons for taking radiographs. When chiropractors refer for radiographic services, 67% refer to medical radiologists and 17% to chiropractic radiologists. Eighty-five percent agreed that chiropractic radiologists are as well qualified as medical radiologists, but 36% thought that medical interpretation carried more legal authority than chiropractic interpretation. Seventy-six percent of respondents thought that the chiropractic radiologist should be consulted only for second opinions. CONCLUSIONS: Most chiropractors obtain radiographs for clinical reasons, such as confirming a diagnosis of pathology, but many continue to use radiography as a screening tool and for medicolegal protection. Prevailing attitudes seem to indicate a need for this specialty in chiropractic, but the chiropractic radiological consultant is not widely used. The disparity between the perceived need for chiropractic radiologists and the current utilization patterns requires further research.

Attitude of Health Personnel↗
PubMed1997

Reversal of accelerated renal allograft rejection with FK 506.

Although FK 506 has been shown to effectively reverse refractory renal allograft rejection, its ability to reverse accelerated renal allograft rejection as a primary agent has not been specifically addressed. Herein evidence of the ability of FK 506 to reverse accelerated renal allograft rejection is presented. A 16-yr-old highly sensitized (PRA 75%) male underwent a second cadaveric renal transplant procedure. Despite induction immunosuppression with ATGAM, cyclosporine, azathioprine, and corticosteroids, a marked elevation in serum creatinine (1.6-->2.1 ng/dl) and reduction in urine output (4000 ml/d-->1000 ml/d) were observed on the sixth post-transplant day. Renal allograft biopsy performed at that time revealed typical features of accelerated rejection including neutrophil margination in glomerular and interstitial capillaries, and C3, IgG, and fibrin deposition in glomerular and interstitial capillaries (by immunofluorescence). FK 506 therapy was promptly instituted and ATGAM therapy discontinued. Serum creatinine peaked within 3 d of FK 506 therapy (2.5 mg/dl) and subsequently progressively dropped to 1.2 mg/dl. Repeat biopsy on FK 506 treatment day 12 revealed marked histologic improvement. Renal function remains excellent (1.3 mg/dl) 18 months after initiation of FK 506 therapy, and recurrent rejection has not been observed. This experience provides evidence that FK 506 therapy may effectively reverse accelerated renal allograft rejection, and that it provides a means for treating antibody-mediated mechanisms of allograft rejection.

Adolescent↗
PubMed1997

Parameters associated with chronic renal transplant failure.

BACKGROUND: Although chronic progressive renal transplant failure (CPTF) is one of the leading causes of end-stage renal disease its exact pathogenesis is still incompletely understood. Histopathological as well as clinical similarities between chronic native kidney diseases and CPTF open the possibility that the latter condition is not exclusively due to a prolonged immunological insult to the grafted organ but also is caused by a mismatch between the metabolic demands of the recipient and the excretory capacity of the transplanted kidney. In this retrospective study we defined clinical parameters which are associated with CPTF. METHODS: Creatinine clearance was followed in 469 patients 45 +/- 0.9 months after transplantation for 2 years. Various immunological and non-immunological parameters were included in an univariate and multivariate regression analysis to define those which are independently associated with CPTF, defined as a decrease of creatinine clearance during the study period. RESULTS: Of all the parameters proteinuria, systolic blood pressure, high Cyclosporin trough concentrations and the cumulative steroid dose were found to be significantly associated with CPTF. A persistent proteinuria of > 2 g/d during the observation period was found to have a positive predictive value of 83% for a deterioration of excretory kidney function of > or = 25% within 2 years. CONCLUSION: In CPTF immunological as well as non immunological factors are independently associated with the decline of excretory allograft function in the late postoperative period.

Blood Pressure↗
PubMed1997

Angiotensin converting enzyme insertion/deletion polymorphism and short-term renal response to ACE inhibition: role of sodium status.

Angiotensin converting enzyme (ACEi) inhibition retards renal function loss, but the therapeutic benefit varies between individuals. Renoprotection is poor in patients with the ACE DD genotype. ACE genotype is reported to affect short-term antiproteinuric response to ACEi, a predictor of long-term renoprotection, in some studies but not in others. Short-term responses to ACEi are enhanced by stimulating the renin-angiotensin system, that is, sodium restriction. We hypothesized that the ACE genotype influences sodium dependency of the response to ACEi. Therefore, we performed a cross sectional analysis of short-term responses to ACEi (enalapril or lisinopril) in 88 patients with stable non-diabetic proteinuria (> 1.0 g/day) and variable sodium intake. ACE genotype distribution was: DD, N = 25; ID, N = 40; II, N = 23. Baseline proteinuria (5.9 +/- 0.7; 5.8 +/- 0.07; 4.8 +/- 0.8 g/day, respectively) and mean arterial pressure (108 +/- 3; 106 +/- 2; 107 +/- 2 mm Hg, respectively) were similar for the three genotypes. ACEi similarly reduced proteinuria (-49 +/- 5; -55 +/- 4, -48 +/- 6%, respectively) and blood pressure (-12 +/- 3; -14 +/- 1 and -12 +/- 2%, respectively) in the three groups. Interestingly, the responses to ACEi of proteinuria (r = 0.42, P < 0.05) and blood pressure (r = 0.41, P < 0.05) correlated with urinary sodium excretion in DD genotype but not in the ID (r = 0.05 and 0.17, resp) or II genotype (r = 0.09 and 0.08, respectively). Thus, in the DD group, individuals with a high sodium excretion had a less effective response to ACEi. We conclude that differences in sodium status could account for disparities between studies on the relationship between ACE genotype and response to ACEi, and that sodium restriction might be a strategy to circumvent treatment resistance in the DD genotype.

Adolescent↗
PubMed1996

Tacrolimus therapy for refractory acute renal allograft rejection: definition of the histologic response by protocol biopsies.

UNLABELLED: Protocol biopsies were performed to define the histologic response to tacrolimus therapy in patients with refractory acute renal allograft rejection. Renal allograft biopsies were performed at defined intervals after initiation of tacrolimus therapy. Protocol biopsies were performed before tacrolimus therapy (within 48 hr of initiation of therapy) and after 1 week of therapy. If the 1-week biopsy did not show rejection reversal, repeat protocol biopsies were obtained at 1- to 2-week intervals, until histologic reversal was observed. Additional biopsies were obtained at 4 weeks and at 8-12 weeks after initiation of tacrolimus therapy. Indicated biopsies were also performed to evaluate increases in serum creatinine. A total of 92 biopsies were performed in 23 patients (average 4.0 biopsies/ patient). Biopsies were performed in each patient immediately before starting tacrolimus therapy (23 biopsies), and 69 biopsies (3.0 biopsies/patient) were performed during tacrolimus therapy. Rejection diagnosis was based on strict Banff criteria. Pretacrolimus biopsies demonstrated mild acute rejection in 64% of patients and moderate acute rejection in 36%. One week after initiation of tacrolimus therapy, protocol biopsies revealed the following: no rejection (60%), improvement (13%), no change (20%), and worsening rejection (7%). Histologic changes at 1 week did not correlate with changes in renal function, as 63% of patients that showed histologic improvement or reversal during the first 2 weeks of therapy did not show improvement in serum creatinine. A lack of histologic improvement (or worsening) at 1 week was demonstrated in a significant proportion of patients (27%); increased tacrolimus dosing provided rejection reversal or improvement in 1-2 weeks in each of these patients. Recurrent rejection was diagnosed on eight biopsies in seven patients, however six episodes were diagnosed by protocol biopsies alone (i.e., in the absence of an elevation in serum creatinine). Delayed improvement in renal function, despite histologic reversal, was likely due to physiologic effects of tacrolimus (i.e., afferent arteriolar vasoconstriction), as histologic evidence of tacrolimus toxicity was not observed during the first 2 weeks of therapy. Histologic evidence of tacrolimus nephrotoxicity (nodular arteriolar hyalinosis) was found in 21% (15 of 69) of biopsies in 39% of patients (9 of 23) at a median time of 60 days (range 12-150 days). Tacrolimus dose and blood levels (by IMx assay) did not correlate with development of clinically silent or clinically evident nephrotoxicity. IN CONCLUSION: 1) protocol biopsies provide information that allows individualization of tacrolimus rejection therapy, 2) histologic resolution of rejection often precedes biochemical improvement, 3) histologic evidence of tacrolimus nephrotoxicity is seldom observed in the first 2 weeks of therapy, and 4) clinically silent recurrent rejection and clinically silent tacrolimus nephrotoxicity are observed with significant frequency during tacrolimus therapy for refractory renal allograft rejection.

Acute Disease↗
PubMed1996

p53-dependent G1 arrest and p53-independent apoptosis influence the radiobiologic response of glioblastoma.

PURPOSE: Loss of the p53 tumor suppressor gene has been associated with tumor progression, disease relapse, poor response to antineoplastic therapy, and poor prognosis in many malignancies. We have investigated the contribution of p53-mediated radiation-induced apoptosis and G1 arrest to the well described radiation resistance of glioblastoma multiforme (GM) cells. METHODS AND MATERIALS: Radiation survival in vitro was quantitated using linear quadratic and repair-saturation mathematical models. Isogenic derivatives of glioblastoma cells differing only in their p53 status were generated using a retroviral vector expressing a dominant negative mutant of p53. Radiation-induced apoptosis was assayed by Fluorescence-activated cell sorter (FACS) analysis, terminal deoxynucleotide transferase labeling technique, and chromatin morphology. Cells were synchronized in early G1 phase and mitotic and labeling indices were measured. RESULTS: Radiation-induced apoptosis of GM cells was independent of functional wild-type p53 (wt p53). Decreased susceptibility to radiation-induced apoptosis was associated with lower alpha values characterizing the shoulder of the clonogenic radiation survival curve. Using isogenic GM cells differing only in their p53 activity, we found that a p53-mediated function, radiation-induced G1 arrest, could also influence the value of alpha and clonogenic radiation resistance. Inactivation of wt p53 function by a dominant negative mutant of p53 resulted in a significantly diminished alpha value with no alteration in cellular susceptibility to radiation-induced apoptosis. The clonal derivative U87-LUX.8 expressing a functional wt p53 had an alpha (Gy-1) value of 0.609, whereas the isogenic clonal derivative U87-175.4 lacking wt p53 function had an alpha (Gy-1) value of 0.175. CONCLUSION: We conclude that two distinct cellular responses to radiation, p53-independent apoptosis and p53-dependent G1-arrest, influence radiobiological parameters that characterize the radiation response of glioblastoma cells. Further understanding of the molecular basis of GM radiation resistance will lead to improvement in existing therapeutic modalities and to the development of novel treatment approaches.

Apoptosis↗
PubMed1996

Renal function and glomerular permselectivity late after living related donor transplantation.

Living related kidney transplantation is the preferable procedure for renal replacement therapy. The aim of the current study was to determine systemic hemodynamic and intrarenal adaptions in donors and recipients late after living related kidney transplantation. Furthermore, glomerular permselectivity was assessed in these subjects. We studied mean blood pressure (MAP), glomerular filtration rate (GFR), renal plasma flow (RPF), microalbuminuria (MIA), 24-hr urinary protein excretion, and glomerular permselectivity (fractional clearance of neutral dextrans [thetaD] as a marker for size selectivity and fractional clearance of dextran sulfate [thetaDS] to assess charge selectivity) in 22 donors and 22 recipients. MAP was normal in the donor group (102 +/- 4 mmHg), but five patients had blood pressure above 140/90 mmHg. This 18%, however, is lower than the prevalence of hypertension in the age-adjusted general population in Austria. The recipients also had normal MAP at the time of study (99 +/- 3); however, 13 needed antihypertensive therapy. GFR and RPF were lower in recipients than in donors (53 +/- 8 vs. 72 +/- 11 and 314 +/- 74 vs. 412 +/- 86 ml/min respectively). In the donor group, GFR was 137 +/- 45% of the expected age-adjusted mean value/kidney due to hyperfiltration. Proteinuria and MIA were higher in the recipients than in the donors (0.39 +/- 0.22 vs. 0.07 +/- 0.04 g/day, 137 +/- 136 vs. 26 +/- 15 mg/day). Nonetheless, five donors had an elevated MIA. A higher need for antihypertensive medication could be observed in recipients with previous rejection episodes, as well as a significantly higher urinary protein excretion and MIA (0.7 +/- 0.42 vs. 0.24 +/- 0.14 g/day, 336 +/- 380 vs. 48 +/- 32 mg/day). ThetaDS was significantly higher in the recipients, whereas thetaDS of the donors was identical to the value obtained from 18 healthy controls (0.7 +/- 0.08 vs. 0.6 +/- 0.06). OD was similar in all groups studied. In conclusion, 76 months after uninephrectomy for renal donation, mild changes in glomerular permselectivity occurred in a subset of donors without affecting renal excretory function. In recipients, proteinuria was due to a defect in glomerular charge selectivity.

Adult↗
PubMed1996

Repression of the insulin receptor promoter by the tumor suppressor gene product p53: a possible mechanism for receptor overexpression in breast cancer.

There is strong evidence to suggest that insulin and insulin-like growth factor (IGF)-I may be important for tumor growth. Both the insulin and IGF-I receptors (IGF-IR) are overexpressed in breast cancer, and antibody blockade of the IGF-IR inhibits the growth of some breast cancer cell lines. Furthermore, expression of an insulin receptor (IR) in a normal mammary epithelia] cell line causes insulin-dependent transformation. Functional inactivation of p53 is also very frequent in many tumors. In this paper, we investigated whether inactivation of p53 might be involved in the overexpression of the IR in malignancy, specifically breast cancer. We demonstrate a positive correlation between IR and IGF-IR levels and p53 overexpression in primary human breast malignancies. To examine possible mechanisms by which p53 may regulate IR gene expression, we show that p53 can repress the IR promoter and that a dominant-negative p53 (248Q) can de-repress the promoter in cells containing normal p53. The p53 effect was shown to be mediated by C/EBP and Sp1 transcription factors. We also documented that p53-null mice had elevated levels of Sp1, but not C/EBPalpha, and that insulin binding to liver extracts was increased compared to wild-type controls. These results suggest that p53 inactivation may lead to an up-regulation of genes, such as the IR, that are dependent on these transcription factors.

Animals↗
PubMed1996

Atubular glomeruli in patients with chronic allograft rejection.

Morphometric studies were performed in 15 patients with chronic renal allograft rejection. Biopsy cores were serially sectioned so that atubular glomeruli could be identified and volumes of individual glomeruli could be measured. Control tissue was obtained from 9 cadaver donors and 8 living donors. Serial sectioning revealed that atubular glomeruli were as common as sclerotic glomeruli in chronic rejection. The prevalence of atubular glomeruli averaged 18 +/- 15% (mean +/- SD) in recipients with chronic rejection, 2 +/- 2% in cadaver donors, and 1 +/- 3% in living donors (P<0.05, recipients vs. donor groups). In comparison, the prevalence of sclerotic glomeruli averaged 19 +/- 13%, 4 +/- 7%, and 7 +/- 10% in the three groups (P<0.05 recipients vs. donor groups). Atubular glomeruli exhibited reduced mean volume (3.1 +/- 0.9 x 10(6)micron(3) vs. 4.5 +/- 1.5 x lO(6)micron(3), atubular vs. open glomeruli in recipients, P < 0.05) but could not be distinguished from open glomeruli by their appearance on single sections. Recipients with chronic rejection exhibited tubular atrophy and interstitial fibrosis with an increase in the interstitial volume fraction to 51 +/- 14% as compared with 29 +/- 6% in cadaver donors and 17 +/- 2% in living donors (P<0.05 recipients vs. donor groups). Similar interstitial expansion was observed in recipients with a high prevalence of atubular glomeruli, recipients with a high prevalence of sclerotic glomeruli, and also in four recipients in whom the predominant form of glomerular injury was transplant glomerulopathy. These results suggest that mechanisms responsible for development of atubular glomeruli are among the processes that contribute to loss of graft function in patients with chronic rejection.

Adult↗
PubMed1996

Characterization and sequence analysis of the human homeobox-containing gene GBX2.

Polymerase chain reaction (PCR) was used to amplify portion of homeobox genes present in a human 11-week fetal brain cDNA library. One of these PCR products was determined by sequencing to be the Gastrulation and brain specific-2 gene (GBX2). Screening this human fetal brain cDNA library with probes specific for GBX2 led to the identification of a 2151-bp cDNA clone. The nucleotide sequence of the cDNA clone encodes for a protein of 347 amino acid residues. The amino acid sequence of the GBX2 homeodomain is identical (100%) to the that of homologous gene, Gbx2, expressed in the developing mouse embryo and virtually identical (97%) to a gene expressed in the developing chicken embryo, CHox7. The 5' end of the GBX2 gene contains a CpG island in the untranslated region and a trinucleotide (CCG)8 repeat in the coding region. The amino-terminal end of the GBX2 protein is proline-rich, with 30 proline residues in one stretch of 120 amino acids. A single 2.2-kb transcript was detected by Northern analysis in the developing human CNS as well as in other tissues. The human genomic clone for GBX2 was also isolated, characterized, and mapped to 2q36(d)-q37 by somatic cell hybrid analysis and fluorescence in situ hybridization. These studies provide a framework for designing future experiments that are needed to determine the functional significance of this gene in CNS development.

Amino Acid Sequence↗
PubMed1996

Cell cycle synchrony unmasks the influence of p53 function on radiosensitivity of human glioblastoma cells.

Although ionizing radiation causes DNA damage that can play a role in tumorigenesis, such irradiation is also an important modality of cancer therapy. We studied the radiation response of the U-87 MG human glioblastoma cell line and transfected derivatives in which p53 function had been inactivated. Although little effect of p53 on the radiation sensitivity of asynchronously growing cultures could be detected, inactivation of p53 resulted in a large increase in clonogenic survival when cells synchronized by mitotic selection were irradiated in early G1. The radiation dose sufficient to reduce cellular clonogenicity by 1 log in cells expressing functional p53 was 3.26 +/- 0.12 Gy, whereas a much higher dose (7.41 +/- 0.44 Gy) was required to achieve the same killing effect in cells in which p53 was inactivated. Apoptosis was excluded as a probable mechanism contributing to the radiosensitivity of these cells. Fluorescence-activated cell sorter analysis, continuous labeling with tritiated thymidine, and time-lapse videomicroscopy documented the first example of a prolonged p53-dependent G1 arrest induced by ionizing radiation during the first postirradiation cell cycle of tumor cells, suggesting a role for G1 arrest in determining the sensitivity of these cells to irradiation.

Cell Cycle↗
PubMed1996

IgA nephropathy histologically resembling focal-segmental glomerulosclerosis: a clinicopathologic study of 18 cases.

IgA nephropathy (IgAN) may present with several histologic patterns, including lesions resembling primary focal-segmental glomerulosclerosis (FSGS). To examine the clinical significance of these lesions, slides from all cases of IgAN diagnosed in our renal biopsy service between 1980 and 1994 for which diagnostic materials were available were reviewed. Eighteen of the 244 cases (7.4%) reviewed showed focal and segmental glomerular sclerosis with capillary collapse, sometimes associated with an overlying "cap" of visceral epithelial cells, and no more than very mild glomerular hypercellularity limited to mesangial areas. All showed mesangial IgA as the major immunoglobulin present by immunofluorescence, and all showed mesangial electron-dense deposits ultrastructurally. The mean age (34.8 +/- 11.0 years [+/- SD]), gender distribution (72% male), and racial distribution (67% white, 17% Hispanic, 11% black, 6% Asian) among the 18 patients with FSGS-like IgAN were similar to those of patients in our population with other histologic lesions of IgAN. Notably, the racial distribution of these patients was different from that of our patients with primary FSGS (> 35% black). Seventy-one percent of patients with FSGS-like IgAN had hematuria, but only one patient had gross hematuria. Eighty-two percent had nephrotic-range proteinuria. The mean serum creatinine (1.6 +/- 1.2 mg/dL; n = 17) and urine protein (5.5 +/- 2.8 g/24 hr; n = 17) levels in these patients at the time of biopsy were not significantly different from mean levels in 42 previously studied patients with primary FSGS (Haas et al, Am J Kidney Dis 26:740-750, 1995). Follow-up data obtained for 11 patients with FSGS-like IgAN (mean follow-up, 70 +/- 25 months; range, 37 to 120 months) showed only one who progressed to end-stage renal failure, with dialysis initiated 74 months postbiopsy. However, renal survival in these 11 patients was not significantly greater than that in the previously studied cohort of primary FSGS patients.

Adolescent↗