T Nadasdy

Johns Hopkins University, Baltimore, MD, United States

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Publications (51)154.09 Total impact

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    ABSTRACT: Pigmented neoplasms are extremely rare in the pancreas, and, when black pigment is identified, it often suggests the diagnosis of metastatic melanoma. The authors describe two patients with pigmented "black" neuroendocrine tumors of the pancreas. One patient had an incidental (0.5 cm) finding, and the second patient had a well-demarcated, 4.5-cm mass identified by computerized tomography that was consistent with an islet cell tumor. The two neoplasms were resected surgically and studied by light microscopy using hematoxylin and eosin (H&E), Fontana-Masson, and iron stains. The neoplasms were examined immunohistochemically, and ultrastructural analysis was performed. H&E stains revealed nests of well-differentiated cells with small, round, centrally placed nuclei. The cytoplasm of the neoplastic cells was pink and granular and contained abundant brown-black pigment. Angiolymphatic and perineural invasion were identified in the larger neoplasm. Both neoplasms demonstrated a positive reaction with a Fontana-Masson stain, which was susceptible to bleaching, and a negative reaction to an iron stain. Immunohistochemical stains showed that neoplastic cells expressed chromogranin and synaptophysin but did not express HMB-45, S-100 protein, glucagon, or insulin. Ultrastructural examination revealed regular neurosecretory granules (100-150 nm) and large, irregularly shaped, electron-dense granules with small lipid inclusions consistent with lipofuscin. These pigmented pancreatic neoplasms are similar histologically and radiographically to the "black adenoma" of the adrenal gland. It is important to recognize these tumors, because they may mimic metastatic melanoma.
    Cancer 10/2001; 92(7):1984-91. · 5.20 Impact Factor
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    ABSTRACT: An association between Bartonella infection and myocardial inflammation has not been previously reported. We document a case of a healthy young man who developed chronic active myocarditis after infection with Bartonella henselae (cat scratch disease). He progressed to severe heart failure and underwent orthotopic heart transplantation. Bartonella henselae, therefore, should be included among the list of infectious agents associated with chronic active myocarditis.
    American Journal of Surgical Pathology 10/2001; 25(9):1211-4. · 4.87 Impact Factor
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    ABSTRACT: Fibrillary glomerulonephritis (FGN) is a rare but progressive glomerular disease usually with end-stage renal disease (ESRD) developing within months or few years following the diagnosis. Little is known about the outcome of renal transplantation in patients with ESRD due to FGN. We report four patients with FGN who received renal allografts. Two patients developed recurrent FGN in their grafts. One patient was diagnosed to have recurrent FGN 9 years post-transplant, and lost his graft 4 years thereafter. Another patient had recurrent disease 2 years post-transplant but has stable graft function after 7 years. One patient died with normal renal allograft function 7 years following transplantation. The fourth patient has chronic transplant nephropathy 34 months post-transplant without evidence of recurrent FGN. A literature review revealed 10 additional patients who received 11 renal allografts due to ESRD caused by FGN. Four of these 10 patients had biopsy-proven recurrence (one patient in two subsequent grafts), but this caused graft loss only in 2 patients 56 months and 7 years post-transplant, respectively. The earliest recurrence was diagnosed 2 years post-transplant. We conclude that although the recurrence rate of FGN in renal transplants is high (around 50%), the recurrent disease has a relatively benign course and prolonged graft survival is possible.
    Clinical nephrology 03/2001; 55(2):159-66. · 1.29 Impact Factor
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    ABSTRACT: In the glomerulonephritides of systemic lupus erythematosus (SLE), the number of subendothelial deposits, when present, generally corresponds to the degree of light microscopic glomerular hypercellularity; only very rarely are no or few such deposits present in cases of focal (WHO class III) or diffuse (WHO class IV) proliferative lupus nephritis. We have recently encountered five cases of active diffuse proliferative glomerlonephritis with no subendothelial and few or no mesangial deposits and thrombotic microangiopathy (TMA) in four patients with SLE and one patient with lupus-like syndrome. Three of the five patients were tested for circulating lupus anticoagulants or anticardiolipin antibodies, and two were positive. All five patients tested negatively for antineutrophil cytoplasmic antibodies (ANCA). Three patients responded to steroid and cyclophosphamide treatment, although one of them died of acute bacterial bronchopneumonia. One patient was lost to follow-up. We conclude that "pauci-immune" proliferative lupus nephritis is rare and should be treated as proliferative lupus nephritis with a proportionate number of subendothelial deposits. The negative ANCA suggests that these cases do not represent incidental ANCA-associated pauci-immune necrotizing and crescentic glomerulonephritis in patients with SLE. Of particular interest is that, in patients with SLE, if associated with TMA, an active proliferative necrotizing glomerulonephritis may be present even in the absence of significant glomerular immune complex deposition.
    American Journal of Kidney Diseases 07/2000; 35(6):1193-206. · 5.29 Impact Factor
  • M G Ripple, D Charney, T Nadasdy
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    ABSTRACT: Renal cholesterol embolization (RCE) in native kidneys has a dismal outcome and frequently leads to irreversible renal failure. RCE may rarely occur in renal allografts as well, particularly if the recipient or the donor has prominent atherosclerosis. The natural history of RCE in renal transplants is unknown. We have reviewed the surgical pathology files of The Johns Hopkins Hospital in the 14-year period between 1984 and early 1999 and found 7 RCE cases among 1500 renal transplant biopsies (0.47%). One of the seven cases had three biopsies showing cholesterol emboli, the first of which was a postreperfusion (immediate posttransplant) biopsy. The probable source of the cholesterol emboli was the recipient in six cases and the donor in one case. Five donors were cadaveric and two were living donors. Six biopsies were taken within the first 4 months posttransplant (four were postreperfusion biopsies). One recent patient had the inciting event of arteriography and stent placement 2 years posttransplant and is currently doing well. One kidney failed due to posttransplant lymphoproliferative disorder (PTLD), another kidney failed with complicating opportunistic infections, and the other five were functioning 2 to 6 years posttransplant. A literature review revealed additional 14 RCE cases in renal transplants. Combining our cases with those in the literature (21 cases), reveals that the origin of the RCE was probably the recipient in 11 cases (seven cadaveric, two living-related, and two unknown), and the donor in 10 cases (eight cadaveric and two unknown). Graft failure occurred in two of the 11 cases, where RCE was of probable recipient origin. Seven of the 10 kidneys, where the RCE was probably of donor origin, failed due to allograft dysfunction; one of them also developed superimposed rejection and cytomegalovirus infection. We conclude that if RCE is originating in the recipient, graft survival is usually good. In contrast, if RCE is of donor origin, graft dysfunction and subsequent graft loss are common. The reason for this difference may be the more extensive RCE developing in an atherosclerotic cadaveric donor during organ procurement or severe trauma leading to death.
    Transplantation 06/2000; 69(10):2221-5. · 3.78 Impact Factor
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    ABSTRACT: A remission in nephrotic proteinuria with steroid treatment appears to favorably alter the natural history of focal segmental glomerulosclerosis (FSGS). It is not known why some patients have a favorable response to steroid treatment whereas others do not. Considering the possibility that differences in the pharmacodynamic responsiveness to steroids among patients might be one factor, the authors examined the relationship between the pretreatment suppressive effect of steroids on lymphocyte proliferation (% inhibition) in vitro and the short- and intermediate-term responses of creatinine clearance (Clcr) and/or nephrotic proteinuria (urine protein/creatinine ratio = Up/c) in 13 patients with FSGS. There were significant correlations between % inhibition and the changes in Clcr at 3 (r = 0.92, p < 0.001) and 6 (r = 0.86, p < 0.01) months and the changes in Up/c at 3 months (r = -0.74, p = 0.02). Thus, the greater the pretreatment lymphocyte steroid sensitivity, the greater the increase in Clcr or decrease in Up/c. The changes in these parameters could not be accounted for on the basis of steroid dose or histopathology. The in vitro sensitivity of FSGS patients' lymphocytes to steroids may be of value in anticipating their clinical response to treatment.
    The Journal of Clinical Pharmacology 02/2000; 40(2):115-23. · 2.84 Impact Factor
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    ABSTRACT: Acute renal allograft rejection is usually seen within the first 3 months posttransplant, and is characterized by an intense infiltrate of T cells. Some acute rejections, however, contain many plasma cells and/or appear late posttransplant. We have investigated 27 cases of intensely plasma cell-rich acute rejections (PCAR) from 1987 to 1997 and have compared them to 21 control cases (CAR) of typical acute rejection. Each group was divided into early (<6 months) and late (>6 months) subgroups. PCAR and CAR cases were matched for histological features of chronic allograft nephropathy. In all four groups, most cases had Banff '97 type IB and IIA acute rejection. A significantly greater number of PCAR cases experienced graft failure due to chronic allograft nephropathy or complications of acute rejection (P<0.05). There was no significant difference between PCAR and CAR in HLA matching, occurrence of posttransplant acute tubular necrosis, presence versus absence of previous allografts, number of previous or subsequent acute rejection episodes, Banff '97 sum scores for acute rejection, cyclosporine A or FK506 levels, or percent change from baseline creatinine at time of biopsy. Plasma cells in PCAR cases showed IgG predominance whereas those in CAR had comparable staining for IgG and IgA. Kappa and lambda light chain immunostaining of all PCAR cases revealed polyclonality. Three of 18 PCAR cases studied for the presence of Epstein-Barr virus RNA showed scattered positivity in 2-7% of lymphoid cells, although the remainder was negative. None of the PCAR cases developed post-transpland lymphoproliferative disorder. We conclude that PCAR can occur from 1 month to many years posttransplant, is associated with poor graft survival, and is not a manifestation of concomitant chronic allograft nephropathy or viral infection, including posttransplant lymphoproliferative disorder.
    Transplantation 10/1999; 68(6):791-7. · 3.78 Impact Factor
  • J A Eustace, T Nadasdy, M Choi
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    ABSTRACT: The Churg Strauss Syndrome is an eosinophil-associated small vessel vasculitis. Although its pathogenesis may be distinctive and the association with severe late-onset asthma typical, the clinical features during the vasculitic phase widely overlap with those of the other forms of necrotizing vasculitis, and no single clinical or histologic feature is pathognomic of the condition. Renal involvement is common, although usually mild, and even when severe it tends to respond well to treatment. The prognosis for both patient and renal survival with adequate treatment is in general good. The optimal treatment strategy, however, is uncertain, and may differ from that for the other vasculitides. In particular, in contrast to Wegener's granulomatosis, the need for routine cyclophosphamide treatment is unconfirmed and requires further study.
    Journal of the American Society of Nephrology 10/1999; 10(9):2048-55. · 8.99 Impact Factor
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    ABSTRACT: Transient intraoperative oliguria is a constant phenomenon during laparoscopic procedures. Laboratory studies have demonstrated that this effect is secondary to a decrease in renal blood flow caused by the pneumoperitoneum. With the advent of laparoscopic harvest of the kidney for renal transplantation, a concern is that increased intra-abdominal pressure may compound the effect of acute cold and warm renal ischemia during transplantation. Acute transient renal ischemia can produce chronic sclerosing histopathologic changes in native kidneys which are similar to those seen in chronic allograft rejection. The effect of positive-pressure abdominal pneumoperitoneum (15 mm Hg) on native kidneys was examined using a rodent model. The effects on renal function and histologic features were also studied. Twenty-four Harlan Wistar-Furth rats were divided into four groups: controls, 1-hour pneumoperitoneum-91-day survival, 5-hour pneumoperitoneum-91-day survival, and 5-hour pneumoperitoneum-7-day survival. Control animals underwent placement of the Veress needle and anesthesia but no induction of pneumoperitoneum. At the time of sacrifice, blood was sampled for serum creatinine measurement. Both kidneys were harvested for frozen and permanent section and stained using hematoxylin and eosin. Specimens were graded for inflammatory and ischemic/sclerotic changes in the interstitium, tubules, glomeruli, and vasculature by a renal pathologist using a histologic score (0-3). In all groups, at a sacrifice interval of either 1 week or 3 months, there were no statistical differences in the histologic score, serum creatinine concentration, or renal weight. In a rodent model, no signs of chronic ischemic histologic changes were detected for a period of 3 months after up to 5 hours of pneumoperitoneum. As well, there was no change in the serum creatinine concentration.
    Journal of Endourology 06/1999; 13(4):279-82. · 2.07 Impact Factor
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    ABSTRACT: The transplantation of kidneys from pediatric cadaveric donors into adult recipients is performed in many centers. However, some studies indicate that the outcome of such renal transplants may be inferior compared with that of adult donors, particularly if the donor is an infant. Morphologic studies of failed pediatric donor kidneys in adult recipients describe various degrees of segmental or global glomerular sclerosis. The authors have performed ultrastructural examinations on such transplants and have identified six cases with diffuse irregular lamellation of the glomerular basement membrane (GBM), a change that may develop as early as 10 weeks after transplantation. The age of all donors was < or =6 years; three were infants. The incidence of the lesion was 9% at our institution in renal transplant patients who received a graft from donors <10 years old. Diffuse GBM lamellation has not been found in renal transplants from adult donors. Light microscopy showed various degrees of diffuse mesangial expansion, usually with segmental glomerular sclerosis. The patients had severe proteinuria. While recurrent focal segmental glomerular sclerosis (FSGS) has to be excluded, such diffuse GBM lamellation is generally not seen in recurrent FSGS cases. The pathogenesis of the lesion is most likely related to hyperperfusion injury of small pediatric donor kidneys grafted into adult recipients.
    American Journal of Surgical Pathology 04/1999; 23(4):437-42. · 4.87 Impact Factor
  • Source
    R Abdi, K Chavin, T Nadasdy
    Nephrology Dialysis Transplantation 03/1999; 14(2):493-6. · 3.37 Impact Factor
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    ABSTRACT: The publication of black and white photomicrographs has a long tradition in pathology. High-resolution film and quality objectives have been the backbone of generating quality photomicrographs suitable for publication. However, the digital imaging revolution has changed the way we view and capture images. As the quality of image capture devices increases and as their price decreases, more and more investigators are using digital imaging, and the use of color digital imaging for teleconferencing, telediagnosis, and reproduction is now well established. The purpose of this study was to determine the file sizes needed to obtain publication-quality black and white images using digital imaging technology. In this study, four experts in renal pathology reviewed 70 black and white images of various file sizes obtained from specimens representing a variety of renal histopathology. Without knowledge of the file size, the four renal pathologists graded the degree of pixelation, and the overall diagnostic and publication quality of the images. In all cases, digital imaging was capable of obtaining publication quality images equal to those achieved using film. The file size needed to achieve publication quality black and white images depended on magnification, with lower magnification images requiring larger file sizes.
    American Journal of Surgical Pathology 12/1998; 22(11):1411-6. · 4.87 Impact Factor
  • J D Kronz, A M Neu, T Nadasdy
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    ABSTRACT: In addition to fibrillary glomerulonephritis (FGN), Congo red negative mesangial fibrils may commonly be seen in sclerosing glomerular diseases. Rarely, these nonspecific mesangial fibrils (NMF) may mimic fibrils in FGN and cause a differential diagnostic pitfall. Following an interesting case of sclerosing crescentic glomerulonephritis with abundant NMF (which is presented in some detail) we have reviewed our renal biopsy files for a period of two and a half years and found additional 16 cases where the presence of NMF warranted studies to exclude FGN and other diseases with fibrillary deposits. The immunofluorescence pattern characteristically seen in FGN was not present in any of these cases. Our data confirm that mesangial fibrillary material seen ultrastructurally in sclerosing glomeruli with negative or nonspecific immunofluorescence (IF) represents a nonspecific reaction of the mesangial matrix to chronic glomerular injury. The presence of NMF should not lead to the erroneous diagnosis of FGN. Negative or nonspecific immunofluoresence, localization to the mesangium in a usually segmental fashion, and the more bundle-like than random arrangement of fibrils are helpful diagnostic hints in differentiating NMF from fibrils in FGN.
    Clinical nephrology 11/1998; 50(4):218-23. · 1.29 Impact Factor
  • Molecular Immunology - MOL IMMUNOL. 01/1998; 35(11):764-764.
  • Transplantation 01/1998; 66(8). · 3.78 Impact Factor
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    ABSTRACT: In a previous study, utilizing antibodies to proliferating cell nuclear antigen (PCNA), we determined the proliferation index (PI) (percentage of PCNA-positive cells) of intrinsic renal cell populations in the normal adult and pediatric kidney. We have found that the PI in both adult and pediatric kidneys was very low (below 0.5 in all examined cell populations). In our present study, we investigated cell proliferation in the developing human kidney with an antibody to PCNA. Histologically normal kidneys were collected from 25 fetuses (spontaneous abortions and stillborns) ranging from 10 wk of gestation to term. Immature mesenchyme (blastema), immature early tubules, ampulla of ureteric bud, proximal tubules, Tamm-Horsfall protein (THP)-positive tubules, distal tubules, collecting ducts, and glomeruli were evaluated separately. The PI for each cell population was calculated. The PI of immature early tubules remains high (33-43) throughout embryonic life. The PI of blastemal cells is initially similarly high, but gradually decreases starting from the second trimester. The PI of THP-positive tubules, distal tubules, collecting ducts, and glomeruli starts out relatively high (5.9, 8.6, 6.0, and 12.4, respectively) and decreases gradually as term approaches (1.8, 1.3, 1.2, and 1.4, respectively). Interestingly, as soon as proximal tubules become differentiated (appearance of light microscopic features of proximal tubular epithelium with TP lectin positive brush border), their PI becomes very low (below 1) irrespective of the age of the kidney. This is the first quantitative study to show changes of the PI in various renal cell populations during human nephrogenesis. These changes in the PI relate to the stage of differentiation of the developing nephron segments.
    Pediatric and Developmental Pathology 01/1998; 1(1):49-55. · 0.86 Impact Factor
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    ABSTRACT: Mast cells (MCs), few in the normal kidney, are found in increased number in the renal parenchyma in diseases associated with persistent chronic inflammation. MCs are not easily identified in routinely processed archival tissue sections with histochemical stains. A more reliable method of detection was provided with the introduction of MC tryptase-specific monoclonal antibodies. To determine the possible role of MCs in renal allograft rejection, we studied 28 biopsy specimens from renal allografts that had been in place for various lengths of time (from 3 days to 40 months) in patients whose primary diagnosis was acute interstitial rejection; the specimens were associated with varying degrees of interstitial fibrosis, edema, and hemorrhage. The specimens were graded on a semiquantitative scale (from 0 to 3+) for the severity of rejection, the degree of interstitial fibrosis, interstitial edema, and interstitial hemorrhage. Eosinophils, plasma cells, and MCs were quantitatively evaluated in these biopsy specimens. MCs were detected by use of a commercially available anti-MC tryptase monoclonal antibody, which proved to be an excellent tool to detect MCs in routinely processed paraffin sections. A positive correlation was found between the number of MCs and the time since transplantation (R = 0.841, P < 0.005) and between the number of MCs and the severity of interstitial fibrosis (R = 0.489, P < 0.005), as well as with interstitial edema (R = 0.517, P < 0.005). MCs were increased in number in patients with moderate (n = 18; mean, 18.00 MCs per 10 high power fields [HPFs]) and severe (n = 5; mean, 12.20 MCs per 10 HPFs) acute rejection compared with patients with mild (n = 5; mean, 2.44 MCs per 10 HPFs) acute rejection and normal kidneys (n = 6; mean, 1.75 MCs per 10 HPFs). These results suggested that MCs might play a role in the process of acute rejection of renal allografts and in the development of interstitial fibrosis.
    Modern Pathology 01/1997; 9(12):1118-25. · 5.25 Impact Factor
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    ABSTRACT: A 43-year-old man with rapidly evolving renal failure from biopsy-proven human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) and superimposed thrombotic microangiopathic changes was treated with prednisone. His serum creatinine decreased from 7.5 to 3.9 mg/dL, and the 24-hour protein excretion decreased from 15.7 to 6.1 g over 6 to 8 weeks. As the prednisone was tapered, however, the creatinine began to increase, and a repeat biopsy was done to assist with therapeutic decisions. The major differences from the pretreatment biopsy were marked reductions in interstitial lymphocytes and macrophages and absence of thrombotic microangiopathic lesions. This is the first report comparing pretreatment and posttreatment renal biopsy specimens and the findings provide some insight into the means by which prednisone exerts its beneficial clinical effects acutely on this disease.
    American Journal of Kidney Diseases 11/1996; 28(4):618-21. · 5.29 Impact Factor
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    ABSTRACT: To determine the nephron segment distribution of tubular epithelial damage and regeneration and the proliferative activity of various nephron segments in human acute tubular necrosis (ATN) with an antibody to proliferating cell nuclear antigen (PCNA) and to compare the findings in native kidneys with ATN with those in transplant kidneys with ATN, archival tissues from 12 native and 21 transplant kidney biopsy specimens and nine transplant nephrectomy specimens were collected that all showed obvious morphological signs of ATN. Nineteen patients with transplant kidneys with ATN were immunosuppressed with cyclosporine and 11 were immunosuppressed with prednisone and azathioprine. There was a predominance of "regenerating" tubules (tubules with thin epithelium) in the distal nephron in native kidneys with ATN; in the transplant kidneys this was less conspicuous. The number of Tamm-Horsfall protein (THP)-positive tubules was decreased in all kidneys with ATN compared with normal human kidneys. In contrast, the number of THP-positive casts was much higher in all kidneys with ATN than in the normal kidneys. In transplant kidneys with ATN the number of THP-positive casts was substantially lower than in native kidneys with ATN. The macula densa appears to maintain its morphological integrity in kidneys with ATN. Both regenerating and normal appearing tubules expressed vimentin and HLA-DR. The proliferation index (PI; ie, percentage of PCNA-positive nuclei) of the renal tubular epithelium in normal control kidneys varied between 0.22 and 0.33, depending on the tubule segment. The highest PI was noted in the transplant kidneys with ATN not treated with cyclosporine (8.0), followed by the native kidneys with ATN (4.4) and the transplant kidneys with ATN treated with cyclosporine (4.3). We did not find any significant difference in the PI between the regenerating (5.0) and normal appearing (5.6) tubules. Proximal tubules (8.7) showed significantly higher PI values than distal tubules (3.5) in transplant kidneys with ATN. Our results show substantial differences between native kidneys and transplant kidneys with ATN. Tubular epithelial cell proliferation in human ATN is prominent and appears to correlate with the severity of ATN. Light microscopically normal appearing tubules and regenerating tubules participate equally in the regeneration of injured tubules. Cyclosporine may have an inhibitory effect on cell regeneration (proliferation) in human transplant kidneys with ATN.
    Human Pathlogy 03/1995; 26(2):230-9. · 2.84 Impact Factor
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    ABSTRACT: Increased proliferative activity of the renal tubular epithelium is thought to be a prerequisite for renal cyst formation by many investigators. However, in humans, the exact in vivo proliferation rate of epithelial cells lining these cysts is not known. In this study, which used immunohistochemical methods with an antibody to proliferating cell nuclear antigen (PCNA), the proliferation index (PI) (percentage of PCNA positive cell nuclei among epithelial cells lining the renal cysts) was determined in 10 cases of autosomal dominant polycystic kidney disease (ADPKD), 8 cases of autosomal recessive polycystic kidney disease (ARPKD), and 8 cases of acquired cystic kidney disease (ACKD). Cysts with proximal and distal nephron phenotype and cysts with markedly thickened basement membranes, as well as cysts lined by atrophic (flattened), "regular" (cuboidal or cylindrical), and hyperplastic epithelium, were evaluated separately. The overall PI of cyst epithelium (excluding hyperplastic cysts) was 2.58 in ADPKD, was 10.5 in ARPKD, and was 3.61 in ACKD. Overall, there were only minor differences in the PI between the various types of cysts. Cysts with hyperplastic epithelium in ACKD (unlike in ADPKD) showed a high PI (9.1). For comparison, the PI of two renal cell carcinomas occurring in two ACKD cases was also determined (13.70 and 8.67%). The PI of tubular epithelium in normal kidneys was only 0.22 to 0.33%, depending on the tubule segment. In contrast, in polycystic kidneys, those noncystic segments of the nephron from which the cysts are thought to originate (distal nephron (specifically collecting duct)) in ARPKD, primarily distal in ADPKD, proximal and distal in ACKD, had PI values similar to those of the cyst epithelium.(ABSTRACT TRUNCATED AT 400 WORDS)
    Journal of the American Society of Nephrology 02/1995; 5(7):1462-8. · 8.99 Impact Factor

Publication Stats

639 Citations
154.09 Total Impact Points


  • 1998–2001
    • Johns Hopkins University
      • Department of Pathology
      Baltimore, MD, United States
    • University of Oklahoma
      Norman, Oklahoma, United States
  • 1999–2000
    • Johns Hopkins Medicine
      • • Department of Pathology
      • • Department of Surgery
      Baltimore, MD, United States
  • 1992–1998
    • Oklahoma City University
      Oklahoma City, Oklahoma, United States
  • 1995–1997
    • University of Oklahoma Health Sciences Center
      • Department of Pathology
      Oklahoma City, OK, United States
  • 1988–1991
    • University of Szeged
      • Department of Pathology
      Szeged, Csongrad megye, Hungary