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S M Bonsib

Publications and source records attributed to S M Bonsib.

At least 19 recordsLinked to original sources
PubMed2001

Polyoma viral infection in renal transplantation: the role of immunosuppressive therapy.

BACKGROUND: Polyoma virus infection in renal transplant recipients has been observed with increasing frequency in recent years. Renal allograft involvement in this condition may occur as a result of primary infection or secondary to reactivation of the latent virus. Interstitial nephritis, ureteric stenosis, rise in serum creatinine and allograft function loss have been attributed to this viral infection. METHODS: In this study we reviewed our experience with 8 patients who developed polyoma viral infection confirmed by allograft biopsy. All patients were receiving mycophenolate mofetil as part of the immunosuppression and 7 of the 8 patients were on tacrolimus. All patients have biopsy proven polyoma viral infection. The following therapeutic maneuvers were carried out following the diagnosis of polyoma viral infection: 1) stopping mycophenolate and 2) switching tacrolimus to cyclosporine or reducing the tacrolimus dose to adjust it at a lower therapeutic trough level. The clinical course and outcome of our patients were reviewed in relation to manipulation of immunosuppressive medications. RESULTS: The incidence of this infection in our transplant program in the last 3 yr was 5.3%. Seventy-five percent of the patients had at least one rejection episode and 63% had more than one rejection episode. The main risk factor for the development of polyoma viral infection was related to the intensity of immunosuppression. The use of antirejection therapy after histological diagnosis of polyoma virus infection was not associated with improvement of renal function despite the histological appearance of acute rejection. Thus, the interstitial nephritis associated with polyoma viral infection appears to be an inflammatory response to the virus rather than acute rejection. Six out of the 8 patients stabilized renal function with reduction in immunosuppression. CONCLUSIONS: Reduction in immunosuppression was associated with the stabilization of renal function when instituted early. However, these patients were left with a degree of allograft dysfunction and their outcome may be significantly compromised. The lack of effective antiviral therapy for polyoma virus may limit the use of newer and more potent immunosuppressive medications.

Acute Disease↗
PubMed2001

The role of the tubulointerstitium in radiation-induced renal fibrosis.

The functional and morphological response of the remaining hypertrophied kidney in unilaterally nephrectomized rats to single doses of 0-20 Gy X rays was investigated. Functional and histological end points were assessed serially 4-24 weeks postirradiation. Renal irradiation led to time- and dose-dependent reductions in renal function, seen in terms of a decreased glomerular filtration rate, increased blood urea nitrogen, and reduced hematocrit. These changes were accompanied by morphological changes in the glomerular, tubular and interstitial portions of the kidney. However, dose-dependent changes were observed only in terms of tubulointerstitial lesions. Significant increases in the degree of interstitial staining for collagen type III and fibronectin were observed 24 weeks postirradiation. These increases in extracellular matrix components were accompanied by a significant increase in interstitial alpha smooth muscle actin, suggesting activation of interstitial fibroblasts into myofibroblasts. There was no evidence of glomerular Tgfb after renal irradiation. A significant increase in tubular Tgfb staining was only seen 8 weeks postirradiation. In contrast, there was a shift of staining to the interstitium such that by 24 weeks postirradiation interstitial Tgfb staining was significantly greater than that seen in controls. These findings suggest that the tubule epithelial cell and the interstitial fibroblast are both active participants in the development and/or progression of radiation-induced renal fibrosis.

Animals↗
PubMed2001

Polyarteritis nodosa.

Polyarteritis nodosa is one of the earliest forms of systemic vasculitis described. It is characterized by segmental necrotizing arterial lesions affecting medium-sized and small-sized arteries. Active necrotizing lesions are frequently associated with chronic reparative lesions. Current convention would exclude patients with necrotizing glomerular lesions from this category. An aneurysm may form when the arterial wall is sufficiently weakened by the necrotizing process. Any organ may be affected; however, pulmonary involvement is very uncommon. Significant potential exists for end organ injury resulting from ischemia, infarcts, and hemorrhage. A variety of other primary systemic vasculitidies, secondary forms, such as connective tissue disease associated, and organ limited forms, have been identified that may exhibit similar arterial lesions including aneurysm formation. Establishing a definitive diagnosis of polyarteritis nodosa is therefore challenging, and mandates dialogue between the pathologist and the clinician primed with pertinent clinical and laboratory data. Fortunately, with early diagnosis and aggressive treatment with cytotoxic agents, the prognosis of polyarteritis nodosa has substantially improved.

Arteries↗
PubMed2000

Acute rejection presenting as nephrotic syndrome.

BACKGROUND: Early diagnosis and treatment of acute rejection is important to prevent continued renal injury. Acute rejection most commonly presents with asymptomatic rise in serum creatinine. Proteinuria associated with acute rejection is well established; however, there is limited documentation of the presentation of acute rejection as nephrotic syndrome in the literature. METHODS AND RESULTS: We report a renal transplant patient who presented with early onset nephrotic syndrome without change in serum creatinine, whose allograft biopsy confirmed acute glomerulitis and vascular rejection. Treatment of the acute rejection was accompanied by resolution of the nephrotic syndrome. A second episode of acute rejection was also manifested as nephrotic range proteinuria. CONCLUSION: The nephrotic syndrome in early post-transplantation period should prompt a work-up for acute rejection even in the absence of the common findings of this complication.

Acute Disease↗
PubMed2000

Renal sinus involvement in renal cell carcinomas.

The renal sinus is the fatty compartment located within the confines of the kidney not delineated from the renal cortex by a fibrous capsule. Because it contains numerous veins and lymphatics, invasion into this compartment may permit dissemination of a tumor otherwise regarded as renal-limited. Thirty-one consecutive renal carcinomas were studied: 22 clear cell renal cell carcinomas (3 multilocular cystic renal cell carcinomas), 4 chromophobe renal carcinomas, and 5 papillary renal carcinomas. The entire interface between the neoplasm and the sinus was embedded. Seventeen carcinomas did not invade the renal sinus and 16 were pT1 or pT2 tumors. Fourteen carcinomas, 13 clear cell renal cell carcinoma and one chromophobe renal carcinoma, invaded the renal sinus fat, and 9 of 14 invaded the lumen of renal sinus veins (all clear cell renal carcinomas). Although 14 of 22 clear cell renal carcinomas appeared to be renal limited pT1 and pT2 cancers, 6 of 14 carcinomas invaded sinus fat and 4 invaded into the lumen of renal sinus veins. Compared with the nine sinus-negative clear cell renal cell carcinomas, the 13 sinus-positive cancers were larger, exhibited more frequent renal capsule and renal vein involvement, and had higher nuclear grades. Renal sinus invasion was most common in clear cell renal cell carcinomas but was uncommon (one in 12) in 3 more indolent renal cell carcinomas: multilocular cystic renal cell carcinoma, chromophobe renal carcinoma, and papillary renal carcinoma. The follow-up period was short (1-17 months), but metastases developed in four of 31 cases. In three cases with metastases, carcinoma had involved the lumen of sinus veins but not the main renal vein, although two of three had also invaded through the renal capsule. This study shows that in carcinomas which appear to be renal limited (pT1/pT2), seven of 23 (30.4%) had invaded sinus fat and four of 23 (17.4%) had invaded sinus veins. We conclude that renal sinus invasion, especially sinus vein invasion, could identify a patient at risk for metastases even in a putative renal limited tumor, and suggest that all cases be examined for this feature. Renal sinus invasion merits further investigation to establish its prognostic importance and possible incorporation into future revisions of the TNM staging system for renal cell carcinomas.

Adult↗
PubMed2000

Acute rejection-associated tubular basement membrane defects and chronic allograft nephropathy.

BACKGROUND: Acute rejection is a major risk factor for chronic allograft nephropathy, although the link(s) between these events is not understood. The hypothesis of this study is that alterations in tubular basement membranes (TBMs) that occur during acute rejection may be irreversible and thereby play a role in the development of chronic allograft nephropathy. METHODS: Fourteen renal transplant patients were selected, each having had two or more biopsies performed (42 total). All biopsies were scored for acute and chronic rejection using Banff 1997 criteria. The initial biopsy showed only acute interstitial rejection (type I rejection). No biopsies contained significant chronic arterial lesions of chronic vascular rejection. The entire cortex was examined on Jones methenamine silver-stained sections at x400 for interruption in TBM staining. The number of tubules with TBM abnormalities was counted, and the renal cortical area was measured by image analysis. Periodic acid-Schiff/immunoperoxidase stain was performed on 12 acute rejection biopsies stained for laminin, cytokeratin 7, CD3, CD20, and CD68. Controls consisted of 11 biopsies (8 negative for rejection and 3 acute tubular necrosis). RESULTS: Numerous TBM alterations in silver staining were identified as being associated with acute rejection and tubulitis, consisting of abrupt TBM discontinuities and/or extreme attenuation with segmental or complete absence of TBM. A loss of TBM matrix proteins was confirmed by absent laminin staining in areas of acute rejection and tubulitis. There was herniation of tubular cells into the interstitium through TBM defects confirmed by cytokeratin staining. The TBM defects were spatially associated with inflammatory cells, particularly macrophages. When the biopsies were divided into two groups, <10 and> 10 TBM breaks/mm2, there were statistically significant morphologic and clinical correlations. The number of TBM disruptions correlated with the serum creatinine at the time of biopsy, a combined Banff t + i score, the difference in tubular atrophy between the initial and most recent biopsy and the difference between the nadir creatinine and most recent creatinine. CONCLUSION: Damage to TBM develops in acute rejection as a consequence of interstitial inflammation and tubulitis. These lytic events correlate with the later development of clinical and morphologic evidence of chronic injury in the absence of arterial injury of chronic rejection. We suggest that chronic allograft nephropathy may have an inflammatory interstitial origin.

Acute Disease↗
PubMed1999

Risk and prognosis in renal neoplasms. A pathologist's prospective.

The incidence of renal carcinoma has increased in the United States over the last two decades. An increased rate of detection of incidental tumors and a variety of exogenous risk factors may be responsible for this increase. Pathologic stage and nuclear grade remain the most important and practical prognostic features, however, the specific tumor type has emerged as important as the cytogenetic validation of recent renal carcinoma classification. Proliferation markers, DNA ploidy, and morphometry have powerful predictive value but are handicapped by cost and complexity. The search continues for molecules of diagnostic and prognostic utility that may also impact invasive and metastatic capability for this group of neoplasms whose course is principally determined by the completeness of the original resection.

Humans↗
PubMed1999

Renal allograft dysfunction associated with cytomegalovirus infection.

Renal transplant recipients are at an increased risk for cytomegalovirus (CMV) infection, which occurs as a primary infection or as a result of reactivation of a latent virus. The main risk factors for symptomatic CMV disease include a CMV-negative recipient of a kidney from a CMV-positive donor (primary infection) and treatment of rejection with monoclonal or polyclonal antibodies. In this study, we report a renal transplant recipient with multiple risk factors for the development of CMV infection. He developed three episodes of CMV disease; the first was associated with gastrointestinal tract involvement, and the second episode was diagnosed according to surveillance laboratory test results in the absence of symptoms. The third episode was associated with acute allograft dysfunction. The renal transplant biopsy specimen showed viral inclusions without acute rejection or glomerular abnormality. Despite the absence of morphological injury on biopsy, treatment of CMV with ganciclovir was accompanied by an improvement in renal function. Further studies are needed to establish the mechanism of allograft dysfunction in the absence of inflammatory changes.

Adult↗
PubMed1999

The Banff 97 working classification of renal allograft pathology.

BACKGROUND: Standardization of renal allograft biopsy interpretation is necessary to guide therapy and to establish an objective end point for clinical trials. This manuscript describes a classification, Banff 97, developed by investigators using the Banff Schema and the Collaborative Clinical Trials in Transplantation (CCTT) modification for diagnosis of renal allograft pathology. METHODS: Banff 97 grew from an international consensus discussion begun at Banff and continued via the Internet. This schema developed from (a) analysis of data using the Banff classification, (b) publication of and experience with the CCTT modification, (c) international conferences, and (d) data from recent studies on impact of vasculitis on transplant outcome. RESULTS: Semiquantitative lesion scoring continues to focus on tubulitis and arteritis but includes a minimum threshold for interstitial inflammation. Banff 97 defines "types" of acute/active rejection. Type I is tubulointerstitial rejection without arteritis. Type II is vascular rejection with intimal arteritis, and type III is severe rejection with transmural arterial changes. Biopsies with only mild inflammation are graded as "borderline/suspicious for rejection." Chronic/sclerosing allograft changes are graded based on severity of tubular atrophy and interstitial fibrosis. Antibody-mediated rejection, hyperacute or accelerated acute in presentation, is also categorized, as are other significant allograft findings. CONCLUSIONS: The Banff 97 working classification refines earlier schemas and represents input from two classifications most widely used in clinical rejection trials and in clinical practice worldwide. Major changes include the following: rejection with vasculitis is separated from tubulointerstitial rejection; severe rejection requires transmural changes in arteries; "borderline" rejection can only be interpreted in a clinical context; antibody-mediated rejection is further defined, and lesion scoring focuses on most severely involved structures. Criteria for specimen adequacy have also been modified. Banff 97 represents a significant refinement of allograft assessment, developed via international consensus discussions.

Acute Disease↗
PubMed1999

Focal-segmental glomerulosclerosis. The relationship between tubular atrophy and segmental sclerosis.

Biopsy specimens with focal-segmental glomerulosclerosis (FSGS) show segmental sclerosis (SS) and tubular atrophy (TA). The relationship between SS and TA was studied using serial sections. Based on the location of the SS, 3 and 5 biopsy specimens, respectively, were classified as FSGS, glomerular tip lesion (GTL) or FSGS, not otherwise specified (NOS). The proximal tubule was classified as normal or atrophic. The glomerulus was tracked through serial sections in both directions and classified as normal, SS (graded 1(+)-4+), or ischemic. Segmental sclerosis was identified in 21 of 24 glomeruli in FSGS, GTL and in 46 of 89 glomeruli in FSGS, NOS; TA was identified in 13 of 16 glomeruli in FSGS, GTL and 6 of 13 glomeruli in FSGS, NOS, which showed 1+ SS, and in 36 of 38 glomeruli in both forms, which showed 2+ to 3+ SS. Basement membrane disruptions at the glomerular-tubular junction and interstitial expansion with inflammation was encountered. Three biopsy specimens with FSGS, NOS had hypertensive changes and showed TA in several normal and in all ischemic glomeruli. Chronic tubular injury is present in most glomeruli containing segmental lesions, even small lesions, suggesting that the glomerular and tubular injury may have a common cause or that tubular injury may result from constituent(s) in the glomerular filtrate.

Adult↗
PubMed1998

Oncocytic adrenocortical neoplasms: a report of seven cases and review of the literature.

Oncocytic neoplasms of the adrenal gland are rare. We describe the clinicopathologic and immunohistochemical findings of seven oncocytic adrenocortical neoplasms, five oncocytomas, and two oncocytic neoplasms of uncertain malignant potential. Three tumors were studied using electron microscopy. These neoplasms occurred in five women and two men (median age, 55 years) with no clinical evidence that the neoplasms were functional. The size of the neoplasms varied from 5.0 cm to 13.5 cm. Histologically, each neoplasm was composed exclusively of oncocytes. The oncocytomas had very low or absent mitotic activity and no evidence of necrosis. The two oncocytic neoplasms of uncertain malignant potential had increased mitotic activity and necrosis but no evidence of invasion or metastases. Nuclear atypia, either focal or generalized, was found in all neoplasms. Immunohistochemical studies performed using fixed, paraffin-embedded sections showed strong reactivity with the mitochondrial antibody mES-13 in all neoplasms. Four of five oncocytomas and one oncocytic neoplasm of uncertain malignant potential expressed keratin, predominantly keratin 18, as shown using the CAM 5.2 and AE3 antibodies. Two neuroendocrine-associated markers, neuron specific enolase and synaptophysin, were positive in seven and five neoplasms, respectively. However, all neoplasms were negative for the other neuroendocrine markers tested, including chromogranin A, tyrosine hydroxylase, and dopamine beta-hydroxylase, as well as for epithelial membrane antigen, S100, and p53. Using the MIB-1 (Ki-67) antibody, proliferative activity was increased in both oncocytic neoplasms of uncertain malignant potential. All six patients with available clinical follow-up data are alive without evidence disease, although the follow-up interval is relatively short (< 2 years) for the two patients with oncocytic neoplasms of uncertain malignant potential. We conclude that oncocytic adrenocortical neoplasms are nonfunctional tumors that can become large before they are detected by radiologic studies. The majority of neoplasms are benign and should not be misdiagnosed as carcinoma.

Adenoma, Oxyphilic↗
PubMed1998

Extensively cystic renal neoplasms: cystic nephroma, cystic partially differentiated nephroblastoma, multilocular cystic renal cell carcinoma, and cystic hamartoma of renal pelvis.

Predominantly cystic renal neoplasms have been the source of diagnostic confusion and controversy. In this review, the authors analyze the clinical and pathological features of four entities that consistently exhibit a diffusely cystic growth pattern, are strikingly similar in their gross appearances, and are not separable by preoperative imaging studies. Based on the literature, this review concludes that tumors in young children that have been classified as cystic nephroma and cystic partially differentiated nephroblastoma likely represent a single entity, and all should be considered highly cystic Wilms' tumors with little or no capacity for invasion or metastasis and diagnosed as cystic partially differentiated nephroblastoma. Conversely, cystic nephroma in adults has no discernible connection with Wilms' tumor or nephrogenic rests and should be considered a benign composite neoplasm of stroma and epithelium of unknown histogenesis, which may rarely become malignant with secondary development of a sarcoma. Multilocular cystic renal cell carcinoma appears to be unrelated to cystic nephroma and if the following criteria are met, it appears to be a neoplasm with an intrinsically cystic growth pattern, and no, or at most little, malignant potential: (1) an expansile mass is surrounded by a fibrous wall, (2) the interior of the tumor entirely is composed of cysts and septa with no expansile solid nodules, and (3) the septa contain aggregates of epithelial cells with clear cytoplasm. Cystic hamartoma of the renal pelvis is a rare, complex tumor composed of stroma with a prominent smooth muscle component and a variety of epithelial elements.

Adenocarcinoma, Clear Cell↗
PubMed1998

Fetal obstructive uropathy without renal dysplasia: a study of the renal findings in 13 cases presenting with megacystis.

PURPOSE: Metanephric maldevelopment is a frequent sequela of fetal urinary tract obstruction, particularly when maternal oligohydramnios and massive lower urinary tract dilatation are present. The kidneys in 13 subjects at an estimated 15 to 39 weeks of gestation with distal urinary tract obstruction presenting with severe megacystis not associated with renal dysplasia were examined to discover other manifestations of impaired renal development. MATERIALS AND METHODS: Complete autopsy specimens in 13 cases of severe megacystis in which 1 and 2 kidneys in 3 and 10, respectively, were free of dysplastic features were examined to determine whether there were abnormalities in the cortex and medulla that indicated impaired renal development. RESULTS: The kidneys in 9 cases had various abnormalities indicative of perturbed renal development, such as the premature disappearance and phenotypic alteration of nephrogenic zone cells, a decreased number of nephron generations and medullary collecting duct abnormalities. In 4 cases the kidneys had developed normally. CONCLUSIONS: The majority of subjects with urinary obstruction but nondysplastic kidneys had significant renal abnormalities that would have limited future functional capacity. However, abnormal development is not inevitable even in severe fetal obstruction, suggesting that select cases may benefit from fetal intervention.

Fetal Death↗
PubMed1997

Renal maldevelopment: a pediatric renal biopsy study.

We reviewed 18 pediatric open renal biopsies performed because of renal insufficiency in patients with renal or renal and lower urinary tract (LUT) anomalies. Nine patients had LUT anomalies, 6 had small kidneys, and 3 had normal-sized, enlarged polycystic, and ectopic kidneys, respectively. Patients with LUT anomalies underwent biopsy at an earlier age and had a higher incidence of extrarenal anomalies. Seventeen biopsy specimens were abnormal: 15 showed focal forms of renal dysplasia, and 1 biopsy each showed glomerulocystic kidney disease and dominant polycystic kidney disease. The specimens with dysplasia also contained normal-looking nephrons, whose numbers were particularly striking in patients with a normal LUT. The biopsy specimen from the ectopic kidney was normal. Progressive renal disease developed in 12 of 17 patients with follow-up. All of them had either bilateral uncorrectable LUT abnormalities or bilateral small kidneys. This study demonstrates that renal biopsies in patients with renal insufficiency and gross abnormalities in kidneys or the LUT will often show evidence of parenchymal maldevelopment, principally focal forms of renal dysplasia Although normal nephrons are also present, and might even predominate, progressive disease should be anticipated in the presence of bilateral involvement because of the underlying developmental abnormality coupled with complications related to LUT disease and deficiency in renal mass.

Biopsy↗
PubMed1996

Angiotensin II receptor antagonists in the prevention of radiation nephropathy.

Angiotensin-converting enzyme (ACE) inhibitors can be used to prevent the development of radiation nephropathy. Current studies were designed to determine whether blocking the angiotensin II (AII) receptor, rather than preventing the creation of AII, would be effective in the prophylaxis of radiation nephropathy. Rats received 17 Gy total-body irradiation (TBI) in six fractions followed by syngeneic bone marrow transplantation (BMT). Prior to TBI the rats were randomized to groups receiving an ACE inhibitor (captopril), an AII type 1 (AT1) receptor antagonist (L-158,809) or no treatment. Renal function was assessed over 40 weeks, and a subset of animals were sacrificed for histopathology at 33 weeks. Renal function deteriorated progressively in animals receiving TBI alone, leading to renal failure by 34 weeks. Renal function was significantly better in animals receiving either captopril or L-158,809, and none of these animals had progressed to renal failure by 43 weeks. Analysis of both renal function and histopathology shows that the AII receptor antagonist is more effective than the ACE inhibitor in the prophylaxis of BMT nephropathy. This indicates that a reduction of activation of the AT1 receptor by AII, by itself, is sufficient for the prophylaxis of radiation nephropathy.

Angiotensin Receptor Antagonists↗
PubMed1996

HMB-45 reactivity in renal leiomyomas and leiomyosarcomas.

Ten renal smooth muscle tumors (seven leiomyomas, three leiomyosarcomas) and an unusual smooth muscle-invested renal cell carcinoma were studied for HMB-45 reactivity. All leiomyomas strongly expressed at least one, and most expressed three, smooth muscle markers (desmin, MSA, SMSA) and were negative for two cytokeratin markers (BDK, AE1). Six of seven leiomyomas and the smooth muscle investment of a renal carcinoma contained a population of cells strongly positive for HMB-45. A total of 15 blocks from the 6 HMB-45-positive leiomyomas were studied, and no adipocytes or abnormal vessels suggestive of angiomyolipoma were identified. The six HMB-45-positive leiomyomas seemed to arise from the renal capsule, whereas a seventh leiomyoma, which was negative for HMB-45, seemed to arise from the renal pelvis. Three leiomyosarcomas were also studied, which strongly expressed at least one smooth muscle marker and contained myofilaments at electron microscopic examination. No cytokeratin reactivity and no HMB-45-positive cells were detected in these leiomyosarcomas nor in the normal renal capsule adjacent to leiomyomas. This study showed that HMB-45-positive cells are detectable in a population of cells in some smooth muscle tumors, particularly in those that appear to arise from the renal capsule.

Actins↗
PubMed1995

Papillary renal tumors. Morphologic, cytochemical, and genotypic features.

BACKGROUND: Papillary renal tumors lack alterations of chromosome 3 and show trisomy of chromosomes 7 and 17, genotypic features distinct from nonpapillary carcinomas. METHODS: The authors examined 39 papillary renal neoplasms to identify morphologic features allowing distinction of high grade from low grade tumors. Twenty-nine papillary tumors and 13 nonpapillary tumors were examined for the presence of trisomy of chromosome 7 using fluorescence in situ hybridization. Data recorded included tumor size, stage, grade, architectural pattern, and the presence of glycogen, foam cells, and iron. RESULTS: Nineteen tumors were classified as low grade and 20 as high grade. The high grade tumors more often formed tall papillae with solid and tubular areas and had more intracellular glycogen, whereas the low grade tumors were more often trabecular. There was no significant difference in tumor size or iron deposition. High grade tumors were of higher stage. Foam cells more commonly were noted in low grade tumors. Sixty-seven percent of low grade, 43% of high grade, and none of the nonpapillary tumors showed trisomy of chromosome 7. Metastases developed only in patients with high grade papillary tumors (10/19, 7 within 2 years of diagnosis), all of whom died of disease. CONCLUSIONS: Papillary renal carcinomas with high nuclear grade are more likely to behave in an aggressive fashion, whereas those with low nuclear grade may be associated with longer disease free survival. Furthermore, trisomy of chromosome 7 can be identified by fluorescence in situ hybridization and is useful in differentiating true papillary from nonpapillary renal neoplasms.

Carcinoma, Papillary↗