INTRODUCTION Foscarnet (trisodium phosphonoformate hexahydrate) is standard treatment for ganciclovir-resistant cytomegalovirus (CMV) infections. In the kidney, foscarnet-induced injury may be attributed to reversible tubulointerstitial lesions, but foscarnet crystals have also been observed within glomerular capillaries, suggesting that foscarnet can lead to glomerular lesions such as crescentic glomerulonephritis. We present biopsy and autopsy findings of foscarnet induced nephropathy in a transplanted kidney, with a particular emphasis on the histopathology and electron micrographic peculiarities of drug crystal deposits. CASE PRESENTATION A 72-year-old Caucasian male patient with a deceased donor kidney was treated with several foscarnet applications due to ganciclovir-resistant CMV infection. Transplant kidney biopsy revealed massive glomerular crystalline precipitates, resulting in crescentic glomerulonephritis and tubular damage. The last foscarnet application was complicated with several infections and kidney graft failure. Autopsy revealed multi-organ damage due to foscarnet crystal precipitations associated with systemic CMV and fungal infection. On autopsy of kidney specimens, we succeeded in preserving the rectangular flat plate-like foscarnet crystals in stacks detected by transmission electron microscopy (TEM) after 100% alcohol fixation. The chemical composition of the crystals was confirmed by attenuated total reflection Fourier transform infrared (ATR-FTIR) spectroscopy. CONCLUSION Transplant kidney biopsy remains the gold standard in distinguishing between foscarnet crystalline glomerular and/or tubulointerstitial lesions, and various forms of rejection and other causes of impaired renal function in transplant kidney.

BACKGROUND The aim of our study was to determine outcomes of standard treatment of antibody-mediated rejection (ABMR) of kidney grafts as compared to the addition of bortezomib or rituximab. METHODS The cohort of this retrospective study included patients treated for ABMR of kidney grafts at our national center in the period of 2005 - 2017, divided into two groups: standard (ST) group treated standardly with plasmapheresis or immunoadsorption, intravenous immunoglobulins, and corticosteroids, and BR group treated with the addition of bortezomib and/or rituximab. Patient and graft survival at 2 years was analyzed by Kaplan-Meier method, and predictors of graft survival were analyzed by Cox regression. RESULTS There were 78 patients with ABMR (48 in the ST group, 30 in the BR group), 41 (53%) were men, mean age 49.5 ± 13.8 years. In ST and BR, respectively, mean serum creatinine was 267 ± 164 and 208 ± 112 µmol/L (p = 0.088), donor-specific antibodies (DSA) were positive in 75% and 97% (p = 0.022), and ABMR was acute in 50% and 33% (p = 0.149). Patient survival at 2 years was 89% in the ST and 100% in the BR group (p = 0.125). Cumulative proportion of kidney graft survival at 1 and 2 years was 67% and 53% in the ST group and 73% and 48% in the BR group, respectively, (p = 0.641). Chronic ABMR (HR 5.22, p = 0.004) was significant, while dialysis dependency at biopsy (HR 3.28, p = 0.072), serum creatinine at kidney biopsy (HR 1.003, p = 0.082), and presence of DQ-DSA (HR 3.37, p = 0.062) were borderline significant predictors of worse graft outcome. Infections were relatively common in both groups, with a trend towards more rehospitalizations due to infections in the first 6 months after treatment in the BR group (p = 0.066). In 5 patients (17%), treatment with bortezomib was discontinued prematurely due to cytopenia. CONCLUSIONS Bortezomib or rituximab, added to standard treatment, did not significantly improve kidney graft survival and was also not associated with significant side effects, except cytopenia in some cases. Treatment of acute ABMR resulted in better graft survival than chronic ABMR.
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AIMS:Kidney biopsy remains the gold standard for accurately diagnosing renal diseases. Urinalysis and assessment of renal function are the cornerstones for assessment of patients prior to biopsy. There is significant overlap in the results of routine urine parameters (proteinuria, erythrocyturia, leukocyturia) among different kidney diseases, which hinders the possibility of adequately estimating disease etiology prior to the biopsy. The aim of our study was to assess whether diverse markers of glomerular and tubular proteinuria - urinary albumin, IgG, α-1-microglobulin (α-1-m) and N-acetyl-β-D-glucosaminidase (NAG) - are capable of distinguishing between patients with primary tubulointerstitial (TID) and primary glomerular disease (GLOM).METHODS:Our study is a retrospective, single-center, consecutive case series of patients referred for kidney biopsy. We analyzed routine urinalysis results performed on a second morning urine sample immediately prior to the biopsy.RESULTS:Patients with TID had significantly higher values of α-1-m and NAG, with lower values of albumin and IgG in the urine compared to patients with GLOM. Three tubular urinary indexes had high sensitivity and specificity for distinguishing TID from GLOM: NAG/albumin, α-1-m/proteinuria, and α-1-m/albumin, with the highest values in the latter index (96.6% and 98.2%, respectively, cut-off point ≥ 0.33).CONCLUSIONS:Prior to kidney biopsy, tubular urinary indexes may present a valuable tool in distinguishing patients with TID from patients with GLOM.
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AIMS:A noninvasive test that foretells kidney graft rejection before loss of kidney function would be desirable. We hypothesized that an increase in estimated protein excretion rate (ePER) from spot urine samples is associated with graft rejection and predicts rejection phenotype.METHODS:151 patients who had undergone first-indication kidney biopsy due to graft dysfunction beyond 3 months after transplant were identified from a national cohort of 616 transplant recipients between 2000 and 2012 (25%). ePER were calculated from spot urine protein-to-creatinine ratios at baseline, 3 months before biopsy (ePER-3m), and at the time of biopsy (ePERbiopsy) and were correlated with histologic biopsy findings.RESULTS:Levels of ePER 3 months before biopsy and at the time of biopsy were greater in 32 patients with antibody-mediated rejection (ABMR) than in 77 patients with T-cell-mediated rejection (TCMR) and 42 patients with other findings (median ePER-3m 912 vs. 320 vs. 232 mg/day/1.73m2; and median ePERbiopsy 1,672 vs. 356 vs. 268 mg/day/1.73m2; p < 0.001). Receiver operator characteristics (ROC) analyses demonstrated that ePER-3m and ePERbiopsy had good diagnostic accuracy to discriminate between biopsy specimens showing ABMR vs. those showing TCMR or other histologic findings (area under the ROC curve 0.84, 95% CI 0.75 - 0.93 and 0.89, 95% CI 0.82 - 0.97, respectively; p < 0.001).CONCLUSIONS:An increase in ePER before kidney graft dysfunction appears to be associated with graft rejection and predicts ABMR phenotype.
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BACKGROUND:Reduction of immunosuppression is a common therapeutic strategy in patients with polyomavirus nephropathy (PVN) but may be associated with acute rejection. This study aimed to evaluate the morphology of PVN in renal biopsies after reduction of immunosuppression.METHODS:Eight of 241 patients who received a kidney transplant between January 2012 and December 2015 presented with BK viremia and biopsy-proven PVN. Morphological evaluation according to Banff criteria and correlation with viremia and kidney function after immunosuppression reduction was performed.RESULTS:PVN grades A and B were diagnosed on average 4.7 months post-transplant in 1 and 7 patients, respectively. Indication biopsies after immunosuppression reduction showed an increase in tubulitis and interstitial inflammation score compared to those at the time of the PVN diagnosis. Surveillance biopsies 1 year after transplantation revealed resolution of interstitial inflammation and tubulitis accompanied by clearance of BK viremia in 4 patients (50%), including 1 patient with rejection. One patient showed residual interstitial inflammation after viral clearance. In these patients, renal function returned to baseline. One patient with persisting low BK virus (BKV) in serum and kidney showed a decrease of tubulointerstitial inflammation but scarring was seen. Rejection occurred in 3 patients (38%).CONCLUSION:PVN-associated interstitial inflammation and tubulitis cannot be differentiated morphologically from T-cell-mediated tubulointerstitial rejection. Significant interstitial inflammation and tubulitis in PVN under low-dose immunosuppression might represent immune reconstitution injury, which is reduced after successful BKV clearance from the serum and kidney. Concomitant rejection in PVN patients on low immunosuppression might be efficiently treated with transient pulse immunosuppressive therapy.
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BACKGROUND:Treatment of idiopathic membranous nephropathy with rituximab was introduced more than a decade ago following experimental data that suggested involvement of B-cell-mediated reactions in its pathogenesis. It was a logical step towards a more selective therapy with less severe side effects as compared to the recommended first-line immunosuppressive therapy with corticosteroids and different immunosuppressant drugs.METHODS:We retrospectively analyzed the anonymous data of patients who were treated with rituximab for idiopathic membranous nephropathy at our institution from January 2006 to July 2016. Daily proteinuria and serum creatinine were analyzed 3, 6, 9, and 12 months after rituximab application. The patients were divided into 4 groups according to proteinuria. We separately analyzed remission rates in the whole group and in groups with different quantity of daily proteinuria. Other history data and laboratory parameters were also compared within different groups of patients.RESULTS:The study involved 29 rituximab treatments in 26 patients: 7 (26.9%) female and 19 (73.1%) male patients. In 16 out of 29 treatment cases (55.1%), patients had been previously treated with cyclophosphamide and steroids, or cyclosporine with low dose of steroids, or both. In 72.4% of patients, antiphospholipase A2 receptor antibodies were present. In 2 cases of treatment (6.9%), patients received rituximab 375 mg/m2 of body surface area in 3 and 4 weekly doses, respectively. In all other cases, repeated rituximab applications were given as needed according to the levels of circulating CD-20 B-cells. The total remission rate in our cohort of patients was 37.9% (11 out of 29 cases). The average serum creatinine in the group of patients who achieved remission was significantly lower than in the group without remission (86.5 vs. 155.5 µmol/L, p = 0.003). There was no difference in the duration of the disease prior to treatment with rituximab between the groups (53.6 and 56.4 months, respectively). The remission rate was highest in the group with daily proteinuria less than 4 g per day (83.3%). There were no remissions in the group of patients with daily proteinuria more than 12 g per day.CONCLUSION:The remission rate after rituximab treatment in our cohort of patients with idiopathic membranous nephropathy was lower than in other studies. The reason for this is possibly the application of a single dose of rituximab in the majority of patients, which might have been insufficient in patients with higher proteinuria.
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Background: Understanding the role of alternative complement pathway dysregulation in membranoproliferative glomerulonephritis (MPGN) has led to a dramatic shift in its classification into two subgroups: immune complex-mediated MPGN and complement-mediated MPGN, consisting of dense deposit disease and C3 glomerulonephritis (C3GN). A limited number of C3GN cases have been published to date with not yet conclusive results since the novel therapeutic approach with eculizumab was introduced.Case presentation: We report the clinical follow-up of a 16-year-old patient in whom a diagnosis of C3GN was confirmed by immunofluorescence and electron microscopy in second and third kidney biopsies, while the first biopsy revealed idiopathic immune complex-mediated MPGN type III, Anders and Strife variant, which failed to improve after several attempts at conventional immunosuppression therapy. Although applied late in an already fairly advanced stage of the severe active form of MPGN, the efficacy of eculizumab on C3GN was evidenced clinically and pathohistologically. Its beneficial influence on pathomorphogenesis was demonstrated by a unique follow-up in the last three biopsies, despite the recent observation, confirmed in this study, of eculizumab binding within the kidney tissue.Conclusions: Clinicians and pathologists should be aware that, in some patients, an underlying genetic or acquired complement alternative pathway abnormality can be masked by an initial immune complex-mediated mechanism, which subsequently triggers an unbalanced excessive continual driving of complement terminal pathway activation and the development of C3GN. In such a patient, supplementary steroids in addition to eculizumab appear necessary to achieve an adequate response.

There are only a few reports of the co-occurrence of acute poststreptococcal glomerulonephritis (APGN) and acute rheumatic fever. We report an unusual case of a 3-year-old boy with nephrotic syndrome and acute renal failure with the transitional need for peritoneal dialysis, biopsy-proven atypical IgA-dominant APGN, and concomitant acute rheumatic fever, successfully treated by steroids. Aggressive treatment with pulses of methylprednisolone proved to be successful and we recommend its use in this type of cases.

Classical Goodpasture's (GP) syndrome is a monophasic illness characterized by pulmonary hemorrhage and rapidly progressive glomerulonephritis with linear IgG deposition along the glomerular and distal tubular basement membrane and destructive necrotizing diffuse extracapillary crescentic glomerulonephritis. The majority of patients have circulating anti-glomerular basement membrane (GBM) antibodies, detectable with standard anti-GBM ELISA. Concurrence of GP syndrome with proliferative glomerulonephritis has only rarely been described. In this report, for the first time we describe in a 21-year-old woman GP syndrome with 50% crescentic sclerosing glomerulonephritis with linear immunofluorescence characteristic of anti-GBM pathogenesis, combined with mixed membranous and membranoproliferative glomerulonephritis with granular immunofluorescence and subepithelial, mesangial and subendothelial deposits characterizing immune complex pathogenesis. The clinical picture was also unusual for GP syndrome, manifesting a recurrent but non-progressive course, nephrotic syndrome, normal renal function and low values of anti-GBM antibodies, identified only by novel more sensitive techniques.

Background: In our previous study on 72 deceased donor renal allograft biopsies, we found that parenchyma thickness/graft length ratio (parenchyma size index - PSI) and resistive index (RI) correlate with histopathology findings in transplanted kidney. Aim: To expand the analysis of correlation of parenchyma size index and resistive index measured by ultrasonography with histopathology findings on renal biopsy. Patients and methods: We analysed 117 deceased donor renal allograft biopsies and respective allograft ultrasounds, performed on 112 patients (66 % men) with mean age of 50 years (range: 21 - 73 years), with kidney graft dysfunction in the years 2010 - 2012. Parenchyma thickness relative to graft length and resistive index were compared with different histopathology diagnoses: acute rejection, chronic rejection, chronic kidney changes, acute tubular necrosis (ATN) and other diagnoses. Results: The mean value of the parenchyma thickness/graft length ratio (parenchyma size index - PSI) and of the resistive index (RI) was 1.45 ± 0.27 (SD) and 0.79 ± 0.10 (SD), respectively. Enlarged PSI was significantly higher in ATN (mean 1.71 ± 0.3) compared with no ATN (mean 1.37 ± 0.24) - p<0.001, and lower when chronic changes were present (mean 1.36 ± 0.24 for chronic changes vs. mean 1.61 ± 0.3 for no chronic changes), p<0.001. In the group without ATN, PSI was enlarged in acute graft rejection compared with no graft rejection (mean 1.48 ± 0.24 vs. 1.25 ± 0.18, respectively) - p<0.001, while in the whole group, that also included ATN, PSI showed no differentiating power for acute rejection, p=0.129. RIwas significantly higher in ATN than without it (mean 0.91 ± 0.1 vs. 0.77 ±0.09, respectively), p<0.001, while RI was not increased (but was actually lower) in acute graft rejection compared to no graft rejection in the group without ATN and in the whole group (mean 0.79 ± 0.1 vs. 0.81 ± 0.11, respectively), p=0.323. Conclusions: Expanded study, on a larger number of biopsies, additionally corroborates our previous observations that parenchyma thickness/graft length ratio is higher in acute tubular necrosis and acute allograft rejection, while resistive index is increased in acute tubular necrosis, but not in acute allograft rejection. Decreased parenchyma thickness/graft length ratio is observed in chronic kidney changes.

Background. A noninvasive screening that foretells acute rejection before loss of kidney graft function might reduce rejection-associated graft damage. We hypothesized that changes in spot urine protein-creatinine ratios (PCR) before acute rejection predict rejection phenotype and graft outcome. Methods. Patients who underwent kidney transplantation between Jan 2000 and Dec 2012 and provided biopsy samples for acute rejection were included. PCR were measured in morning spot urine at baseline (PCRbaseline) and 3 months before biopsy (PCR-3m). We investigated whether changes in PCR between baseline and 3 months before rejection (DPCR=PCR-3m-PCRbaseline) were predictive of distinct rejection patterns and graft loss. Results. In the observed period 616 patients were transplanted, of whom 103 (17%) had acute rejection >3 months post-transplant. The median ΔPCR was 20 (IQR 8 to 38) mg/mmol and median percent ΔPCR was 100 (IQR 40 to 226)%. The absolute and relative ΔPCR progressively increased with higher pathohystological degree of rejection.Table: No Caption available.Receiver operator characteristics analysis demonstrated that ΔPCR had good diagnostic accuracy to predict antibody-mediated rejection (area under the curve 0.82) and ΔPCR >120% had the best sensitivity and specificity (82% and 70%, respectively). After a median follow-up of 6.2 years, 29 patients lost their graft. The incidence of graft loss was higher in patients with ΔPCR >100% (40% vs. 16%, P=0.005). In multivariate analysis, patients with ΔPCR >100% had an increased risk of graft loss (hazard ratio 3.4, 95% CI 1.2-9.6; P=0.019), independently of recipient and donor age, graft function, and rejection phenotype. Conclusion. An increase in proteinuria before acute kidney graft rejection is a predictive marker of antibody-mediated or mixed rejection and could be used as a surrogate marker for poor outcomes.

BACKGROUND:It has been suggested that C1q and immunoglobulin M (IgM) nephropathy are variants of minimal change nephrotic syndrome (MCNS). Many researchers believe that these two conditions signify a worse prognosis for children with MCNS in comparison with immunofluorescence (IF)-negative MCNS. The aim of our study was to determine the prognostic significance of C1q nephropathy and IgM nephropathy in children with MCNS.METHODS:Fifty-five children with MCNS who had been biopsied over the course of 24 years at our institution were retrospectively categorized into three groups on the basis of IF microscopy findings: IF-negative MCNS (29/55 patients), MCNS with IgM nephropathy (19/55 patients), and MCNS with C1q nephropathy (7/55 patients). Clinical characteristics at disease presentation, clinical course, and renal outcome were compared between groups during the median follow-up period of 16.9 years (minimum 1.0, maximum 31.1 years).RESULTS:No statistically significant differences in clinical characteristics at disease presentation, clinical course, and renal outcome were found. Children with IgM nephropathy, C1q nephropathy, and IF-negative MCNS were clinically indistinguishable.CONCLUSIONS:We concluded that C1q or IgM nephropathy variants do not seem to signify a worse prognosis in children with MCNS in comparison with IF-negative MCNS.

Hypocomplementemic urticarial vasculitis syndrome (HUVS) is a rare immune-complex small vessel systemic vasculitis involving kidney in about 50% of patients. Characteristic clinical features are recurrent urticaria, decreased serum complement, skin vasculitis, arthritis, eye inflammation, abdominal pain, glomerulonephritis and positive anti-C1q antibodies. We report a 36-year-old woman with a 12-year history of recurrent urticaria and 2 years of urticarial vasculitis. On admission, she also had arthritis, pleuritis and pericarditis, abdominal pain, pathologic urinalysis, low serum values of C3, C4 and CH50. All immunoserology was negative except for ANA 1:80 and anti-C1q 620 IU. 'Full-house' immune complex vasculitis was demonstrated in skin and lung biopsies. A kidney biopsy showed diffuse proliferative segmental active and sclerosing glomerulonephritis with mesangial and endocapillary proliferation, neutrophil exudation, necrosis, extracapillary crescents and segmental and global glomerulosclerosis. 'Full-house' glomerular and extensive extraglomerular vascular and tubulointerstitial immune deposits with dominant IgG, C3 and C1q were noted by immunofluorescence. Electron microscopy revealed electron dense deposits with an ultrastructural 'fingerprint' pattern in the glomerular mesangium, transmembranous in capillary walls and in the arteriolar wall. Our patient fulfilled the criteria for HUVS and SLE, in accordance with the not infrequent clinical and immunoserological overlapping of the two diseases.

Hypocomplementemic urticarial vasculitis syndrome (HUVS) is a rare immune-complex small vessel systemic vasculitis involving kidney in about 50% of patients. Characteristic clinical features are recurrent urticaria, decreased serum complement, skin vasculitis, arthritis, eye inflammation, abdominal pain, glomerulonephritis and positive anti-C1q antibodies. We report a 36-year-old woman with a 12-year history of recurrent urticaria and 2 years of urticarial vasculitis. On admission, she also had arthritis, pleuritis and pericarditis, abdominal pain, pathologic urinalysis, low serum values of C3, C4 and CH50. All immunoserology was negative except for ANA 1:80 and anti-C1q 620 IU. ’Full-house’ immune complex vasculitis was demonstrated in skin and lung biopsies. A kidney biopsy showed diffuse proliferative segmental active and sclerosing glomerulonephritis with mesangial and endocapillary proliferation, neutrophil exudation, necrosis, extracapillary crescents and segmental and global glomerulosclerosis. ’Full-house’ glomerular and extensive extraglomerular vascular and tubulointerstitial immune deposits with dominant IgG, C3 and C1q were noted by immunofluorescence. Electron microscopy revealed electron dense deposits with an ultrastructural ’fingerprint’ pattern in the glomerular mesangium, transmembranous in capillary walls and in the arteriolar wall. Our patient fulfilled the criteria for HUVS and SLE, in accordance with the not infrequent clinical and immunoserological overlapping of the two diseases. Hypocomplementemic urticarial vasculitis syndrome (HUVS) is a rare immune-complex small vessel systemic vasculitis involving kidney in about 50% of patients. Characteristic clinical features are recurrent urticaria, decreased serum complement, skin vasculitis, arthritis, eye inflammation, abdominal pain, glomerulonephritis and positive anti-C1q antibodies. We report a 36-year-old woman with a 12-year history of recurrent urticaria and 2 years of urticarial vasculitis. On admission, she also had arthritis, pleuritis and pericarditis, abdominal pain, pathologic urinalysis, low serum values of C3, C4 and CH50. All immunoserology was negative except for ANA 1:80 and anti-C1q 620 IU. ’Full-house’ immune complex vasculitis was demonstrated in skin and lung biopsies. A kidney biopsy showed diffuse proliferative segmental active and sclerosing glomerulonephritis with mesangial and endocapillary proliferation, neutrophil exudation, necrosis, extracapillary crescents and segmental and global glomerulosclerosis. ’Full-house’ glomerular and extensive extraglomerular vascular and tubulointerstitial immune deposits with dominant IgG, C3 and C1q were noted by immunofluorescence. Electron microscopy revealed electron dense deposits with an ultrastructural ’fingerprint’ pattern in the glomerular mesangium, transmembranous in capillary walls and in the arteriolar wall. Our patient fulfilled the criteria for HUVS and SLE, in accordance with the not infrequent clinical and immunoserological overlapping of the two diseases.

Currently used diagnostic criteria in different endemic (Balkan) nephropathy (EN) centers involve different combinations of parameters, various cut-off values and many of them are not in agreement with proposed international guidelines. Leaders of EN centers began to address these problems at scientific meetings, and this paper is the outgrowth of those discussions. The main aim is to provide recommendations for clinical work on current knowledge and expertise. This document is developed for use by general physicians, nephrologists, urologist, public health experts and epidemiologist, and it is hoped that it will be adopted by responsible institutions in countries harboring EN. National medical providers should cover costs of screening and diagnostic procedures and treatment of EN patients with or without upper urothelial cancers.

BACKGROUND:The aim of our study was to evaluate the prognostic value of glomerular and tubular proteinuria and tubular enzymuria as early indicators of therapeutic response to induction therapy with i.v. pulse cyclophosphamide (CyC) and methylprednisolone (MP) in patients with antineutrophil cytoplasmic antibody (ANCA) associated glomerulonephritis.METHODS AND FINDINGS:An observational single-center study was conducted in 30 patients with ANCA-associated glomerulonephritis. Patients were divided into subgroups with good or poor response to CyC therapy according to clinical and laboratory parameters. The diagnosis of ANCA-associated glomerulonephritis was based on the Chapel-Hill disease definitions. Good response to induction therapy was significantly associated with higher absolute values of urine N-acetyl-beta-D-glucosaminidase (NAG) to creatinine ratio (above 14.83 microcat/mol) and urine immunoglobulin G (IgG) to albumin ratio (above 0.09) at the time of diagnosis, while albuminuria or proteinuria did not have any early predictive value. The remission of renal disease was anticipated as early as 3 months after introduction of induction therapy in patients with reduction of urine NAG to creatinine ratio below the baseline value and in patients with at least 24% rise in eGFR.CONCLUSIONS:Urine IgG to albumin and urine NAG to creatinine ratio are better early predictors of treatment response in patients with ANCA-associated glomerulonephritis than proteinuria or albuminuria.

Hantaviruses can be associated with severe form of hemorrhagic fever with renal syndrome although there are only a few cases reporting chronic kidney disease after hantavirus infection. We report a severe nonresolving chronic renal failure after protracted Dobrava hantavirus infection successfully treated with corticosteroids. Ten days after working in a basement a 33-year-old man fell seriously ill, with high fever, chills, diffuse myalgia, headache and abdominal pain. After hospital admission a diagnosis of hemorrhagic fever with renal syndrome caused by Dobrava hantavirus was made. Acute oliguric kidney injury developed in the first 3 days after admission, in a few days diuresis restored and he became polyuric. Nevertheless renal failure persisted and he needed hemodialysis. Because of nonresolving kidney failure, nephrogenic diabetes insipidus and renoparenchymal arterial hypertension persisting 2 months after onset of symptoms, a kidney biopsy was performed, showing severe necrotizing tubulointerstitial nephritis. High dose methylprednisolone therapy was started and his renal function significantly improved. Two months later a second renal biopsy showed persisting elements of active necrotizing tubulointerstitial nephritis. We decided to stop corticosteroid treatment and introduced aldosterone antagonist eplerenon as anti-fibrotic agent, and his renal function further improved and remained stable. Nine months later his serum creatinine concentration was 227 mu ol/L, proteinuria 0.156g/day and well controlled nephrogenic diabetes insipidus.

Background. Until now studies have shown conflicting results about morphologic and hemodynarnic parameters in predicting histopathology results in renal graft malfunction. We sought to analyze whether parenchymal thickness relative to graft length and resistive index (RI) measured by ultrasonography can predict histopathology findings on renal biopsy.Patients and Methods. We retrospectively analyzed 72 deceased donor renal allograft biopsies and respective allograft ultrasounds, performed on 68 patients (57% men) with mean age of 50 years (range, 21-73), with kidney graft dysfunction in 2010 and 2011. Parenchymal thickness relative to graft length and RI were compared with different histopathology diagnoses: Acute rejection, chronic rejection, chronic kidney changes, acute tubular necrosis (ATN), and other diagnoses.Results. The mean value of the RI and of the parenchymal thickness/graft length ratio (parenchyma size index [PSI]) was 0.81 +/- 0.10 (SD) and 1.48 +/- 0.27 (SD), respectively. Enlarged PSI was significantly higher in ATN (mean 1.72 +/- 0.26) compared with no ATN (mean 1.39 +/- 0.23; P < .001), and lower when chronic changes were present (mean 1.40 +/- 0.25 for chronic changes vs mean 1.62 +/- 0.28 for no chronic changes; P = .004). In the group without ATN, PSI was enlarged in acute graft rejection compared with no graft rejection (mean 1.50 +/- 0.24 vs 1.24 +/- 0.13, respectively; P < .001), whereas in the whole group, including ATN, PSI showed no differentiating power for acute rejection (P = .526). RI was significantly higher in ATN than without it (mean 0.91 +/- 0.10 vs 0.79 +/- 0.08, respectively; P < .001), whereas the RI was not increased (but was actually lower) in acute graft rejection compared with no graft rejection, neither in the whole group (mean 0.81 0.09 vs 0.82 +/- 0.12, respectively; P = .611).Conclusions. Enlarged parenchymal thickness/graft length ratio on ultrasonography was observed in ATN and acute allograft rejection. The RI was increased in ATN, but not in acute allograft rejection. Decreased parenchymal thickness/graft length ratio was observed in chronic kidney changes.