Post-operative complications of tibial plateau fractures treated with screws or hybrid external fixation.

PURPOSE: To assess the complications and second surgeries rates at 1 year follow-up in a group of patients underwent minimally invasive fixation with screws or hybrid external fixation (HEF) for tibial plateau fractures (TPF). The hypothesis was that low Schatzker (I-IV) TPF would have shown a lower complication rate with respect to high Schatzker (V-VI) TPF. METHODS: 148 patients who underwent minimally invasive surgery with screws or HEF for TPF were included and pooled in two groups: mono-condylar (Schatzker I-IV) and bi-condylar (Schatzker V-VI). The rate of second surgeries and complications, such as stiffness, infection, wound dehiscence and malunion occurred within 1 year, were reported. RESULTS: Statistically significant difference between mono-condylar and bi-condylar groups was found in terms of stiffness (18% vs. 37%, p = 0.01), malunion (4% vs 21%, p = 0.004) and second surgeries (32% vs. 48%, p = 0.049). Associated procedures performed during TPF fixation increased risk of second surgeries (OR 2.1, p < 0.001). No differences in terms of second surgeries and complications were found in bi-condylar group treated with screws and HEF. CONCLUSION: Bi-condylar TPF treated with minimally invasive surgery developed a significantly higher rates of stiffness, malunion and second surgeries within 1 year compared to mono-condylar fractures. Moreover, when an associated procedure was performed, the risk of a reoperation was nearly doubled. Trial registration number PG 0012506 CE AVEC 620/2018/Oss/IOR.

Migration of the femoral component and clinical outcomes after total knee replacement: a narrative review.

Loosening is considered as a main cause of implant failure in total knee replacement (TKR). Among the predictive signs of loosening, migration is the most investigated quantitative parameter. Several studies focused on the migration of the tibial component in TKR, while no reviews have been focused on the migration of the femoral component and its influence on patients' clinical outcomes. The aim of this narrative review was (1) to provide information about of the influence of migration in femoral component of TKR prostheses, (2) to assess how migration may affect patient clinical outcomes and (3) to present alternative solution to the standard cobalt-chrome prostheses. A database search was performed on PubMed Central® according to the PRISMA guidelines for studies about Cobalt-Chrome femoral component migration in people that underwent primary TKR published until May 2020. Overall, 18 articles matched the selection criteria and were included in the study. Few studies investigated the femoral component through the migration, and no clear migration causes emerged. The Roentgen Stereophotogrammetric Analysis has been mostly used to assess the migration for prognostic predictions. An annual migration of 0.10 mm seems compatible with good long-term performance and good clinical and functional outcomes. An alternative solution to cobalt-chrome prostheses is represented by femoral component in PEEK material, although no clinical evaluations have been carried out on humans yet. Further studies are needed to investigate the migration of the femoral component in relation to clinical outcomes and material used.

Two different posterior-stabilized mobile-bearing TKA designs: navigator evaluation of intraoperative kinematic differences.

PURPOSE: The purpose of this study was to compare two types of posterior-stabilized (PS) mobile-bearing (MB) total knee arthroplasties (TKAs). The hypothesis was that no major differences were going to be found among the two TKA designs. METHODS: Two cohorts of patients who were divided according to implant design (Cohort A, new design gradually reducing radius PS MB TKA; Cohort B, traditional dual-radius PS MB TKA) were analyzed by means of intraoperative navigation. All operations were guided by a non-image-based navigation system that recorded relative femoral and tibial positions in native and implanted knees during the following kinematic tests: passive range of motion (PROM), varus-valgus stress test at 0° and 30° (VV0, VV30) and anterior/posterior drawer test at 90° of flexion (AP90). RESULTS: There were no significative differences in kinematic tests between the two implants. Cohort A, however, showed a different post-implant trend for VV0 and VV30 that were lower than the pre-implant ones, as expected, while for Cohort B, the trend is opposite. However, the gradually reducing radius prosthesis (Cohort A) showed a trend of improving stability (29% compared to the preoperative status) in mid-flexion (VV30) which the traditional dual-radius design (Cohort B) would not. Moreover, we found no differences among postoperative results of the two TKA designs. CONCLUSION: Despite design variations, no difference has been found among the prostheses in terms of PROM, rotations and translations. Both design kinematics did not show paradoxical external rotations, but an increase in femoral translation in mid-flexion without affecting the functioning of the prosthesis. LEVEL OF EVIDENCE: II.

[Proteomics and the kidney: an innovative approach to the study of renal disease]. / Proteomica e rene: un approccio innovativo allo studio delle malattie renali.

In the post human genome era, several ''omics'' fields are emerging. Proteomics has experienced a rapid growth in the recent past and has great potential for the future. Proteomic technologies are used with increasing frequency also in nephrology. The aim of this review is to examine the recent application of emerging proteomic technologies to the study of renal physiology and pathophysiology. We highlight the use in renal research of a number of available techniques including 2-dimensional gel electrophoresis, liquid chromatography/mass spectrometry, surface-enhanced laser desorption/ionization, and capillary electrophoresis/mass spectrometry. We examine the role, efficacy and diagnostic potential of the different proteomic approaches, focusing on current difficulties and potential solutions. The integrating role of bioinformatics and the need for standardized procedures for sample preservation and analysis and reporting of results are also discussed. Although the field is still in an embryonic stage, the knowledge gained up to now is important not only for a better understanding of renal physiology and pathophysiology, but also for the identification of disease markers and the development and follow-up of new therapies. This review gives an overview of proteomics, providing background information, outlining the scopes, highlighting the applications in nephrology, and reporting advantages and limitations.

Expression of platelet-derived growth factor receptors in normal and diseased human kidney. An immunohistochemistry and in situ hybridization study.

We studied the expression of PDGF-alpha and -beta receptors in 10 normal and 40 pathologic human kidneys (five minimal change disease, five membranous nephropathy, 25 IgA nephropathy, five lupus nephritis), by both immunohistochemistry and in situ hybridization techniques. In normal-appearing kidneys, both PDGF-alpha and -beta receptors were expressed at the glomerular and interstitial level, the latter receptor more intensely than the former. The distribution and degree of expression of both receptors in nonproliferative glomerulonephritides were comparable with those found in normal-appearing kidneys. PDGF-beta receptor gene and protein expression were upregulated in proliferative nephritides both at the glomerular and the interstitial level and strictly correlated with the grade of histologic lesions. Finally, PDGF beta receptor expression was observed at a low level in normal-appearing renal vessels, and strikingly increased in injured arteries. Diseased kidneys displayed only a slight increase of PDGF-alpha receptor expression, chiefly at the interstitial level. Noteworthy, a few cases of lupus nephritis showed a moderate increase of PDGF-alpha receptor also at the glomerular level. These data establish PDGF-beta receptor activation as a candidate for driving glomerular and interstitial proliferation and, probably, expansion of extracellular matrix in proliferative glomerulonephritis, while the role of PDGF-alpha receptor activation at the renal level remains to be elucidated.

Taking Care of Relationships in the Intensive Care Unit: Positive Impact on Family Consent for Organ Donation.

BACKGROUND: Organ donation refusal from relatives of potential donors with brain death significantly reduces organ availability. The need for organ donation has increased over time, but the shortage of available donors is the major limiting factor in transplantation. We analyzed the impact of a new systematic communication approach between medical staff and patients' relatives on the rate of consent to organ donation. METHODS: The study was conducted as a single-center, non-randomized, controlled, before-and-after study at an 18-bed intensive care unit (ICU) of a university hospital. We compared the rate of consent for organ donation before and after the introduction of the new communication approach. RESULTS: A total of 291 brain-dead patients were studied. The consent rate increased from 71% in the pre-intervention period (2007-2012) to 78.4% in the post-intervention period (2013-2015), with an 82.75% increase in the 2014 to 2015 period. During these periods, no significant variation of consent to organ donation was recorded at the national and regional levels. CONCLUSIONS: The introduction of a new communication approach between medical staff and relatives of brain-dead patients was associated with a significant increase in the rate of consent to donation. Our results highlight the importance of empathy with relatives in the ICU.

Double J stent with antireflux device in the prevention of short-term urological complications after cadaveric kidney transplantation: single-center prospective randomized study.

The placement of a double J stent to protect a uretero-vesical anastomosis in a kidney transplant is a widespread procedure performed to reduce the incidence of fistula and stenosis at the anastomosis. However, the presence of a double J stent may cause vesicoureteral reflux (VUR), predisposing one to urinary tract infections (UTIs), which may be a significant source of morbidity for the graft. We evaluated whether a ureteral stent incorporating an antireflux device can reduce the incidence of ureteral reflux and UTIs. From January to December 2003, 44 kidney transplant recipients were randomized to receive a 14-cm 4.8-F double J stent with (group A) or without an anti-reflux device (group B). Primary end points were the reduction of the incidence of VUR and of UTIs. The secondary end point was the graft function, on the basis of mean serum creatinine level at 3, 6, and 12 months. We failed to observe statistically significant differences in terms of either the incidence of VUR and UTIs, or the short-term outcomes of the grafts. We concluded that the anti-reflux device does not have an impact on the incidence of stent-related side effects.

[Identification of an objective reference parameter for the reconstruction of a large incisional hernia following physiological principles]. / Identificazione di un parametro obiettivo di riferimento per la ricostruzione secondo criteri fisiologici del grande laparocele.

Repairing a parietal defect of a large incisional hernia should not be limited to the closure of the breach by means of the modern biocompatible prosthetic sheets, but must also be able to restore a correct intra abdominal pressure, otherwise the derangement from the normal respiratory dynamics and the circulatory stasis in the abdominal veins and in those of the lower limbs remain unaltered. Over-correcting the parietal abdominal tension on the contrary can cause a dangerous compartmental syndrome. The attempts of an intraoperative measurement of the correct intra abdominal pressure restoration has been generally hampered from the condition of curarization of the patient during the operation. Using the automatic mechanical ventilator fixed at volume and not at pressure priority, as usual, can offer the possibility to calibrate, following objective parameters, the propriety of the surgical repair still during the final phases of the reparative operation. The simplicity and ingenuity of the here proposed method and the normal availability in every operative theatre of the necessary means for this measurements described, requires attention among the surgeons and a large diffusions of its simple use.

Insulin resistance and hypoglycemia in a patient with systemic lupus erythematosus: description of antiinsulin receptor antibodies that enhance insulin binding and inhibit insulin action.

We studied a patient with systemic lupus erythematosus and type B insulin resistance, who progressed from extreme insulin resistance to fasting hypoglycemia. The plasma insulin level was 63.3 +/- 20.9 pmol/L in the fasting state and rose above 1440 pmol/L postprandially. Intravenous administration of human insulin caused almost no decline in plasma glucose. Therefore, it was concluded that the patient was still resistant to insulin and that plasma insulin did not play a crucial role in the development of hypoglycemia. Immunoglobulin G from this patient did not inhibit insulin binding to the insulin receptor; rather, it enhanced [125I]insulin binding in both the immunoprecipitate and the in vitro binding assay to intact cells. Antiinsulin receptor antibodies strongly inhibited insulin internalization in human adipocytes, slowed down the dissociation of [125I]insulin from receptors and failed to induce down-regulation of surface insulin receptors in both the presence and absence of insulin. Finally, autoantibodies mimicked the insulin stimulatory effect on human fat cell lipogenesis even after long term exposure, but inhibited the metabolic potency of insulin when added simultaneously with the natural ligand. We conclude that antiinsulin receptor antibodies induce fasting hypoglycemia, through their continuous receptor stimulatory action, and insulin resistance, possibly by a conformational perturbation of the receptor protein, which, in turn, uncouples insulin receptor binding from receptor function.

Protease-activated receptor 1 and plasminogen activator inhibitor 1 expression in chronic allograft nephropathy: the role of coagulation and fibrinolysis in renal graft fibrosis.

BACKGROUND: Chronic allograft nephropathy (CAN), the major cause of renal graft failure, frequently displays extensive interstitial fibrin deposition. Little is known in regard to the cause of the altered coagulation/fibrinolysis balance and its relevance in the pathogenesis of CAN. Thrombin, present within the fibrin clots, can interact with a specific receptor, protease-activated receptor 1 (PAR-1), and modulate a variety of cell functions. On the other hand, the derangement of the fibrinolytic system may directly affect extracellular matrix (ECM) degradation. METHODS: In the present study, we investigated, by in situ hybridization, PAR-1 gene expression and the mRNA levels for tissue factor and plasminogen activator inhibitor 1 (PAI-1), two key regulatory molecules of coagulation and fibrinolysis, in 16 CAN biopsies and in 10 normal human kidney grafts. The thrombin-induced transforming growth factor beta (TGF-beta) gene and protein expression in proximal tubular cells (PTC) was investigated by Northern blotting and ELISA, respectively. RESULTS: Fibrin deposits, absent in normal grafts, were observed in the interstitial space and arterial wall of CAN. Tissue factor gene expression was not increased either at the vascular or at the interstitial level in CAN. On the contrary, PAI-1 gene expression, barely detectable in control tissue, was strikingly increased in CAN, with a distribution resembling the pattern of fibrin deposition. Note that PAI-1 gene expression was directly correlated with the degree of interstitial fibrosis. In addition, fibrin deposits were strictly associated with a marked increase of PAR-1 gene expression in endothelial cells and PTC. The tubular expression of PAR-1 was significantly higher in Banff grade II-III than in grade I. In vitro, incubation of PTC with thrombin caused a significant up-regulation of TGF-beta gene expression, followed by an increased TGF-beta release into the supernatant. Interestingly, urine from CAN patients contained significantly higher levels of TGF-beta. CONCLUSIONS: Fibrin deposits in CAN may result from the increased expression of PAI-1 and the subsequent inhibition of fibrinolysis. The reduced fibrinolysis may cause, in turn, a decreased ECM turnover. Finally, thrombin, preserved in the active form within the fibrin clots, may interact with PAR-1 highly expressed on PTC and induce an up-regulation of ECM deposition in a TGF-beta-dependent manner.

Interference of angiotensin-converting enzyme inhibitors on erythropoiesis in kidney transplant recipients: role of growth factors and cytokines.

BACKGROUND: Recent data indicate that factors other than erythropoietin (EPO), such as insulin-like growth factor 1 (IGF-1), can promote erythropoiesis in vitro and correct the anemia of chronic renal failure in vivo. IGF-1 is produced by the liver under growth hormone control, as well as by other sources, including the kidney. The erythropoietic role of growth factors and cytokines and their possible modulation by angiotensin-converting enzyme inhibitors (ACEI) has never been explored. METHODS: This study evaluated the serum levels of EPO, IGF-1, interleukin (IL)-2, IL-3, and granulocyte macrophage-colony-stimulating factor in 40 kidney transplanted patients with or without posttransplant erythrocytosis (PTE) and in 10 living kidney donors. Then, the effect of ACEI therapy on the above pattern was examined in patients with PTE. RESULTS: EPO and IGF-1 serum levels were significantly higher in patients with PTE than in patients without PTE and in living kidney donor subjects. ACEI therapy significantly reduced hematocrit (Hct) as well as circulating IGF-1 and EPO levels. Of note, the decrease in IGF-1 was prominent mainly in those patients whose EPO levels were not significantly modified by ACEI therapy. In all of the patients Hct levels displayed a direct relationship with circulating IGF-1 levels, but not with EPO concentration. Growth hormone did not significantly differ among the groups examined, whereas it steeply increased under ACEI. Finally, no significant difference in IL-2, IL-3, and granulocyte macrophage-colony-stimulating factor serum levels was detected. CONCLUSIONS: IGF-1 seems to play a role in the ACEI-related decrease of Hct in patients with PTE, chiefly in patients without any modification of EPO serum levels.

Immunologic evaluation during the first year of life of infants born to cyclosporine-treated female kidney transplant recipients: analysis of lymphocyte subpopulations and immunoglobulin serum levels.

BACKGROUND: In rodents, CsA has been shown to affect T-cell development, giving rise to an abnormal production of mature T cells and the absence of many T-cell subsets as well as to autoimmunity. Surprisingly, only a few studies investigated the effect of the immunosuppressive drug on the immune system of the human fetus. METHODS: We examined six infants born to female kidney transplant recipients who had received cyclosporine and methylprednisolone throughout their pregnancies. Peripheral blood was obtained 1 day and 2, 4, 6, and 12 months after birth, and two-color flow cytometric immunophenotyping of lymphocytes was performed. RESULTS: Total T cells, as well as CD4+ and CD8+ T cells, were low at birth, but normalized thereafter. Among T-cell activation markers, the expression of CD25, the alpha chain of the interleukin-2 receptor, was below the normal range or low range throughout the study period, and HLA-DR expression was extremely low at birth and failed to increase up to 12 months. The number of total B cells was lower than normal at birth, but steeply increased over time. In contrast, B-cell subset bearing CD5 antigen was severely depleted throughout the first year of life. Total IgG concentration was significantly lower than in controls at 2 months, mainly because of subnormal levels of IgG1 and IgG3 subclasses, which remained in the low range up to 6 months. Finally, infants showed normal numbers of true natural killer (NK) cells (CD3-CD16+CD56+), whereas the expression of CD57 antigen, defining non-MHC-restricted cytotoxic lymphocytes, was barely detectable at birth and failed to increase over time, in both CD8+ and CD8- subsets. Of note, none of the infants had clinical evidence of an immunodeficient state. CONCLUSIONS: continuous exposure to CsA in utero seemingly impairs T-, B-, and NK-cell development and/or maturation, and most of its effects are still apparent at 1 year, which might suggest that conventional vaccinations should be delayed in these infants.

Cultured human mesangial cells produce both type 1 and type 2 plasminogen activator inhibitors.

Cultured human mesangial cells (HMC) derived from normal kidneys have been shown to synthesize tissue-type plasminogen activator (t-PA) and excess amounts of PA inhibitor type 1 (PAI-1). Conflicting results have been obtained concerning the production of urokinase-type PA (u-PA) and efforts to show PA inhibitor 2 (PAI-2) met with failure. We evaluated the fibrinolytic profile of cultured HMC lines obtained from 12 patients with renal carcinoma and one cadaveric kidney donor. Subconfluent cells (third passage) were incubated overnight in serum-free medium. t-PA, u-PA, PAI-1 and PAI-2 antigens were assayed by ELISA methods and PA and PAI activities by amidolytic methods both in conditioned medium (CM) and cell extracts (CE). Besides PAI-1, PAI-2 antigen was detected in all but one HMC lines. At variance with the former, which was largely released in the culture medium, PAI-2 was mainly cell-associated. t-PA antigen was found in all but two cell lines while u-PA antigen was detected in relatively high concentrations in 8 cell lines. PA activity, identified as u-PA by functional and immunological criteria, was measured in CM of six of the eight u-PA producing cell lines, whereas PAI activity was undetectable or very low in CM of all cell lines, suggesting that PAI-1 was largely inactive. Functional assays of cell extracts demonstrated the presence of PA activity, again identified as u-PA, only in samples (five lines) containing u-PA antigen in excess over PAI-2. PAI activity was found instead in the extracts in which the inhibitor was higher than the activator (six lines) and was identified as PAI-2, as it inhibited u-PA but not single-chain t-PA and was neutralized by a polyclonal anti-PAI-2 antibody. The heterogeneous fibrinolytic pattern of HMC lines was confirmed by mRNA analysis of three representative lines. Results were similar when HMC lines at passage five were used, except that the u-PA content was significantly reduced both in CM and CE. These findings indicate that the fibrinolytic profile of cultured HMC is more complex than previously reported. The production of large amounts of PAI-2 may represent an additional control mechanism of proteinase activity.

Pregnancy in renal transplantation: immunologic evaluation of neonates from mothers with transplanted kidney.

The occurrence of pregnancy in young female organ transplant recipients may sustain a high risk for prematurity and low rate of malformations in neonates. Therefore, it is necessary to counsel couples who want a child. In case of pregnancy, strict guidelines must be observed. Continuous exposure to CsA in utero seems to impair T-, B- and NK-cell development and function in neonates. This effect is prolonged throughout the first year of life. In addition, low levels of serum immunoglobulins occur at the same time. This leads to suggest a delayed administration of classical vaccinations (after the first 6 months of life) in view of the potential risks of both sub-optimal immunologic responses, and adverse events after the administration of live, attenuated vaccines in infants born from young female organ transplant recipients.

Extreme insulin resistance due to anti-insulin receptor antibodies: a direct demonstration of autoantibody secretion by peripheral lymphocytes.

A 59-year-old woman with systemic lupus erythematosus was found to have marked hyperglycemia, extreme insulin resistance and abnormally high plasma immunoreactive insulin. Her circulating erythrocytes displayed a dramatic decrease of 125I-labeled insulin binding. Both the whole serum and purified IgG fraction strongly inhibited the binding of radiolabeled insulin to control erythrocytes. These results suggested, although indirectly, the existence of antibodies to insulin receptors in the serum of the patient. To directly investigate this issue, we used an enzyme-linked solid-phase immunoassay which allows the detection and enumeration of lymphocytes secreting antibodies towards insulin receptors. Peroxidase-conjugated anti-human immunoglobulin is used to reveal the binding of antibodies to insulin receptor-coated dishes. We demonstrated that the patient's mononuclear cells, when briefly incubated in Petri dishes with partially purified insulin receptor, were able to secrete immunoglobulins of G class specifically directed to the antigen. Moreover, only a fraction of the whole population of anti-insulin receptor antibodies was directed towards the insulin binding region of the receptor, seemingly corresponding to the auto-antibodies detected with conventional binding-inhibition assay.

Rare phenotype and transplantability in cadaveric kidney transplant.

The waiting list for kidney transplants in the Apulia region contains recipients (about 30%) who were never selected for transplant due to the rare HLA antigen phenotypes and homozygosis. Therefore, an algorithm was selected to equilibrate the chance for patients to be selected despite a rare phenotype. We calculated for each patient, the sum (%) of the A, B, DR antigen frequency (total phenotypic frequency; TPF). All the potential recipients were grouped into five classes in increasing order of TPF. The number transplanted depended on the phenotype frequency. The selection index was the quotient of the number selected and the total number of patients. The selection index was 0.28 to 0.43 to 0.79 to 1.34 to 2.38 from class 1 to 5. To equilibrate the transplantability of rare phenotype recipients on the waiting list, a bonus was introduced for the most disadvantageous frequency class. Adding the bonus modified the selection index as follows: 1.0 to 1.25 to 1.5 to 1.34 to 2.38, which appears more equilibrated except for the class 5. In conclusion, if a bonus is applied for rare phenotypes, the chance to be transplanted becomes similar between patients with other parameters the same.

Experience with cyclosporine: approaching the therapeutic window for C2 levels in maintenance kidney transplant recipients.

This study was aimed to evaluate the clinical benefit of C2 monitoring in 191 stable renal transplant patients previously monitored by C0. All patients had been transplanted for at least 1 year and received cyclosporine (CsA)-based immunosuppression since the start. At the inceptions C0 levels were significantly correlated with C2 values (P<.0001). Patients with starting C2 levels >1000 ng/mL showed significantly higher levels of serum creatinine (sCr) both at inception (1.66 +/- 0.50 vs 1.44 +/- 0.41 mg/dL; P=.0021) and at the end of a 2-year follow-up (1.84 +/- 0.80 vs 1.46 +/- 0.51 mg/dL; P=.005). C2 monitoring revealed that a high percentage of patients were overexposed to CsA, mainly in the subgroup with most recent renal engraftments (12 to 24 months). The switch to C2 monitoring was associated with a slower deterioration of graft function (P=.02). Further, the mean values of C2 over a 2-year follow-up were inversely correlated with sCr at the end of follow-up (P=.0005). Finally, patients with mean threshold C2 levels above 720 ng/mL, roughly corresponding to the median value of C2, showed significantly lower levels of sCr at the end of follow-up (P=.0004). In conclusion, C2 monitoring of maintenance renal transplant patients allows one to identify a significant percentage of overexposed subjects, possibly limiting the rate of progression of chronic graft dysfunction. Target range values between 700 and 900 ng/mL appear to be associated with better long-term kidney graft function.

[Correlation between the onset of early proteinuria and the outcome of renal transplantation. Experience of a single centre]. / Correlazione tra insorgenza di proteinuria precoce e decorso clinico del rene trapiantato. Esperienza di un singolo centro.

BACKGROUND: Proteinuria is associated with an increased risk of renal failure. In chronic kidney transplant failure it is associated with poorer graft outcome. MATERIALS AND METHODS: In our Unit 405 renal transplants were performed between April 1992 and December 2001. We analysed 1) the main causes of post-transplant proteinuria and 2) the prognostic significance for graft outcome in patients with a minimum follow-up of 6 months. RESULTS: Early proteinuria was associated with a higher incidence of chronic allograft nephropathy (CAN) and de novo/recurrent nephropathies. Graft outcome was poorer in patients with early persistent proteinuria. CONCLUSIONS: Proteinuria after renal transplantation increases the risk of graft failure. We can, therefore, hypothesize that a graft biopsy is the best way to reveal the causes of proteinuria so that therapeutic interventions, which have been shown to reduce proteinuria, can be applied immediately.

[Recurrent and de novo glomerular disease after renal transplantation]. / Recidive della nefropatia di base e nefropatie "de novo" in pazienti portatori di trapianto renale.

The development and progression or recurrent and de novo renal disease does not seem to have been influenced by the use of newer immunosuppressive agents. The rate of development of recurrent and de novo renal disease has been variable and is perhaps related to pre-existing immunological and/or haematological factors. The diagnosis of recurrent glomerulonephritis requires an accurate diagnosis of both primary renal disease and subsequent disease in the transplant kidney. Published data suggest that recurrent glomerulonephritis occurs in 6 to 19.4% of all renal transplant recipients, and causes the loss of 1.1 to 4.4% of all renal allografts. However, the propensity for glomerulonephritis to recur seems to be time dependent. Consequently, as grafts survival increases, so, too, does the likelihood of disease recurrence. In conclusion, currently available data on recurrence patterns of the less common nephropathies are unfortunately inadequate and our practice is therefore guided by small series, case reports, and local experience. It is to be hoped for that this deficit be addressed in the near future through the use of powerful database and registries, some of which are prospectively collecting data on specific disorders. Prospective studies on the treatment of recurrent glomerulonephritis are lacking. As grafts last longer and recurrent glomerulonephritis becomes a more significant entity, affecting greater numbers of patients, the opportunity to study management prospectively will be possible. This will probably require a cooperative, multicentre approach but it is clearly the only way forward, remembering that renal transplantation is a treatment, not a cure.