Can Doppler Ultrasonographic Indices of the Renal Artery Predict the Presence of Supernumerary Renal Arteries?

Background

Variations of the renal arteries, including the presence of supernumerary renal arteries, are important to be identified prior to renal transplant. Angiography has been the gold standard test for the pretransplant evaluation of the renal vasculature. However, this modality is expensive and invasive. The aim of this study was to assess whether Doppler ultrasonographic (DU) indices of the renal artery could predict the presence of supernumerary renal arteries.

Methods and materials

Retrospectively, we analyzed multidetector computed tomography angiography (presence or absence of the supernumerary renal artery), DU (peak systolic velocity, resistive index, pulsatility index, end-diastolic velocity, and acceleration time) findings of 30 healthy potential renal transplant donors. Recipient operator characteristic (ROC) curves were used to examine the predictive values of the available DU indices for supernumerary renal arteries.

Results

The mean age of donors was 28.4 ± 4.1 years. Of 60 kidneys evaluated, a supernumerary renal artery was found in 10%. The ROC curve analysis revealed an area under the curve of noninformative (below 0.5) for all DU parameters, indicating that none of the studied parameters could predict the presence of a supernumerary renal artery.

Conclusions

Although the smaller diameter of the main renal artery has previously been found to predict the presence of supernumerary renal arteries, the present study revealed that DU indices of the renal artery may not indicate the presence of supernumerary renal arteries.     

Do the Abnormal Results of an Implantation Renal Biopsy Affect the Donor Renal Function?

Background

Living kidney donation has become an important source for renal transplantation. Thus, renal function after donation is an important issue. In this study, we examined histological abnormalities in implantation biopsy specimens from living kidney donors and analyzed the renal function of the remaining kidney.

Methods

Using the 2007 Banff classification system, we analyzed 121 kidneys from living donors who underwent implantation biopsies (IBs) between 2010 and 2011. Donor characteristics, intraoperative factors, and perioperative renal functions, such as serum creatinine and glomerular filtration rate (GFR), were evaluated. Univariate and multivariate regression analyses were performed to identify the factors related to each histological abnormality and postoperative 1-year donor renal function.

Results

Most histological abnormalities in healthy living donors were scored as 1 on the Banff scale. Univariate and multivariate analyses revealed that donor age was the only preoperative factor related to tubular atrophy (odds ratio [OR] = 1.104; P = .012) and glomerular sclerosis (OR = 1.050; P = .019). Intraoperative factors were not related to histological parameters. And histological abnormalities did not affect postoperative 1-year renal function. In contrast, donor age, preoperative GFR, and estimated blood loss were significantly related to 1-year postoperative GFR.

Conclusion

Most histological abnormalities in healthy living donors were minor. The incidence of abnormalities correlated with donor age. However, postoperative renal functions in living donors were not affected by histological abnormalities. Larger-scale investigations with long-term follow-up analysis will be needed.     

Microalbuminuria—A Biomarker of Renal Microvascular Disease

Microalbuminuria (amount greater than 30–300 mg/day) reflects an abnormal glomerular capillary permeability to protein. It is usually dependent upon three mechanisms. First, loss of negatively charged surface of the glomerular capillary wall secondary to circulating toxic substances injury—namely, oxidative stress and proinflammatory cytokines—allows the albumin with negatively charged surface to freely escape into the urine. Second, intraglomerular hypertension and hemodynamic maladjustment secondary to glomerular endothelial dysfunction increases filtration pressure and enhances sized selective proteinuria leakage. Third, podocyte injury leads to a vicious cycle of hemodynamic maladjustment and endothelial and podocyte injuries. All three of these mechanisms induce glomerular endothelial injury and microalbuminuria, which reflects renal microvascular disease.     

Renal actinomycosis—An unusual cause of a renal abscess

We report an uncommon case of a renal abscess with actinomycosis infection in a 59-year-old female, who had stage 5 chronic renal disease and type 2 diabetes mellitus. Abdominal computed tomography revealed an enlarged right kidney infiltrated with multiple cyst-appearing lesions of homogeneous, low density contents. A nephrectomy was performed because of persistent toxic signs after treatment with antibiotics. The patient was well 1 year following surgery. We also review previous cases reported in the literature.     

Case Report: Treatment of Renal Artery Aneurysms by Ex Vivo Renal Artery Aneurysm Repair and Transplantation

Background

Renal artery aneurysms are increasingly being detected incidentally during diagnostic imaging using magnetic resonance imaging, computed tomography, or angiography performed for evaluation of other diseases. Our understanding of their natural history and surgical management has evolved significantly during the past two decades.

Treatment of Immunoglobulin A Nephropathy Recurrence Post–Renal Transplant

Immunoglobulin A nephropathy (IgAN) is the most commonly occurring glomerulonephritis. Recurrence of disease in the transplanted kidney can significantly reduce allograft survival rates. Currently, there is no definitive management plan for IgAN recurrence in a transplant that reduces the rate of decline of allograft function and prolongs time to dialysis or re-transplantation. Herein we present a 48-year-old man who had received a renal transplantation in 2006 following his diagnosis of IgAN. In 2015, the patient was noted to have an elevated blood pressure and proteinuria (urinary protein:creatinine ratio [uPCR] 170 mg/mmol). A transplant biopsy confirmed recurrent IgAN. A year later, he presented with dipstick hematuria, nephrotic-range proteinuria (uPCR 820 mg/mmol), and a serum creatinine of 90 to 140 μmol/L. A second biopsy revealed mesangioproliferative glomerulopathy consistent with crescentic IgAN. An optimal management plan is currently unknown for recurrent crescentic IgAN in the transplanted kidney. We decided to treat this patient with oral cyclophosphamide daily and high-dose prednisolone. The treatment has so far yielded a positive response and managed to preserve allograft function without significant adverse effects for our patient. Our case illustrates the importance of timely biopsies to identify recurrence of disease and highlights an effective therapeutic option for recurrent IgAN with crescent formation in a transplant.     

Renal phosphate handling of premature infants of 23–25 weeks gestational age

Premature infants with low serum phosphate concentrations (<2 mmol/l) are at risk for osteopenia. Therefore, serum phosphate levels in premature infants should be kept above 2 mmol/l. Premature infants of 26-31 weeks gestational age (GA) have renal phosphate threshold concentrations (Tp/GFR) in the range of normal serum phosphate values (2 mmol/l). Therefore, these infants show significant urinary phosphate excretion only when serum phosphate levels are normal, and urinary phosphate excretion can be used to monitor phosphate supplementation. However, few data are available on extremely premature infants of 23-25 weeks GA. The objective of this study was to compare Tp/GFR levels in infants of 23-25 weeks GA to those in infants of 26-31 weeks GA. We retrospectively evaluated case notes of 12 infants of 23-25 weeks GA and compared them to 19 infants of 26-31 weeks GA. Tp/GFR was calculated from simultaneous measurements of urinary phosphate, urinary creatinine, serum phosphate, and serum creatinine. Tp/GFR values 3-5 weeks postnatally were lower in infants of 23-25 weeks GA (1.06+/-0.36 mmol/l, p<0.001) than in infants of 26-31 weeks GA (1.76+/-0.26 mmol/l). Near term (35-37 weeks postmenstrual age), there was no significant difference between Tp/GFR values in infants of 23-25 weeks GA (1.83+/-0.32 mmol/l) and in infants of 26-31 weeks GA (2.05+/-0.22 mmol/l). We conclude that at 3-5 weeks postnatally, infants of 23-25 weeks GA are at risk for low Tp/GFR values, leading to urinary phosphate excretion even in the presence of low serum phosphate levels. In these infants, serum phosphate levels should be monitored, and phosphate supplementation should be adjusted to keep serum phosphate levels above 2 mmol/l.     

Is the Graft Function of Living Donor Renal Transplants Associated With Renal Mass Matching by Computed Tomography Angiographic Volumetry?

Background

Donor renal volume, which can be easily measured by computerized tomographic angiography with 3-dimensional reconstruction, may influence graft outcomes. Low functional renal mass and donor kidney–recipient body size mismatch can lead to progressive renal injury and poor graft function.

Materials and methods

This single–center retrospective analysis of 51 consecutive living donor renal transplantations performed between January 2005 and December 2011 defined transplant renal volume per unit recipient body surface area (BSA; mL/m²). The patients were divided into 2 groups: group I (n = 31, donor–recipient BSA ratio ≤1) and group II (n = 20, BSA ratio >1). We analyzed the clinical characteristics and laboratory data of donors and recipients to ascertain correlations with, renal volumes and graft outcomes.

Results

The renal volumes of living donors correlated with estimated glomerular filtration ratios (eGFR; r = .314, P = .025). Serum creatinine after renal transplantation correlated with transplanted renal volume at 1, 3, and 12 months (r = −.319, P = .048; r = −.407, P = .010; r = −.472, P = .002). Serum eGFR also correlated with transplanted renal volume at 3 and 12 months after renal transplantation (r = .318, P = .049 and r = .388, P = .015). There were no significant differences between groups for acute or chronic rejection, infection or delayed graft function. However, serum creatinine levels were higher (P = .011, P = .022, and P = .007) and serum eGFR significantly lower in group I at 1, 3, 6, and 12 months after renal transplantation (P = .036, P = .042, P = .042, and P = .049, respectively). There was no significant difference in graft survival.

Conclusions

Renal volume of living donors may reflect renal function and have a significant impact on graft outcomes. Renal volume matching should be considered to select donor–recipient pairs for living donor renal transplantation.     

Renal parenchymal malacoplakia: a different stage of xanthogranulomatous pyelonephritis?

Malacoplakia is a rare inflammatory condition characterized by demonstrative Michaelis-Gutmann bodies, which are foamy histiocytes with distinctive basophilic inclusions. Malacoplakia is caused by the inadequate elimination of bacteria by macrophages or monocytes as a result of defective phagocytic activity. Xanthogranulomatous pyelonephritis is characterized by the destruction of renal parenchyma and its replacement by solid sheets of foamy lipid-laden macrophages. Prolonged infection of the kidney, which is frequently caused by an obstruction of the urinary tract, is the pathologic mechanism of that condition. We present a 6-year-old patient with a poorly functioning kidney who had a prolonged recurrent urinary tract infection. The results of histologic analysis revealed an inflammatory infiltration consisting predominantly of foamy and epithelioid histiocytes that contained round intracytoplasmic concretions characteristic of Michaelis-Gutmann bodies. We suggest that malacoplakia might be a stage of xanthogranulomatous pyelonephritis.     

Possible Effects of Interferon-α on Fas-Induced Renal Apoptosis in Mouse

Fas (APO-1/CD95) is a cell surface receptor that initiates apoptotic pathway. Fas-stimulated ROS generation may play important role in Fas-mediated apoptosis. The aim of this study was to evaluate the influence of interferon-α on oxidative stress parameters in Fas-induced renal apoptosis in mice kidney. Subjects and methods. One-month-old Balb C male mice were used for the study. The animals were divided in four groups: group 1 were the controls, group 2 mice were treated with anti-Fas antibody i.p., group 3 mice were treated with IFN‐α, and group 4 mice were treated with both agents simultaneously. The mice were killed 48 h afterwards, and kidneys were homogenized. TBA reactive substances (TBARS), glutathione content, and reactive carbonyl group (RCG) were measured. Results. The results showed a statistically significant increase of TBARS (p < 0.05) and RCG (p < 0.05) concentration in the group treated with anti-Fas antibody versus control. IFN-α decreased the concentration of TBARS and RCG after anti-Fas antibody administration (p < 0.05). There is no significant difference in glutathione content between investigated groups. Conclusion. IFN-α might be considered as a new target for therapeutic intervention in FasL/Fas induced renal injury.     

Renal Production,Uptake, and Handling of Circulating αKlotho

αKlotho is a multifunctional protein highly expressed in the kidney. Soluble αKlotho is released through cleavage of the extracellular domain from membrane αKlotho by secretases to function as an endocrine/paracrine substance. The role of the kidney in circulating αKlotho production and handling is incompletely understood, however. Here, we found higher αKlotho concentration in suprarenal compared with infrarenal inferior vena cava in both rats and humans. In rats, serum αKlotho concentration dropped precipitously after bilateral nephrectomy or upon treatment with inhibitors of αKlotho extracellular domain shedding. Furthermore, the serum half-life of exogenous αKlotho in anephric rats was four- to five-fold longer than that in normal rats, and exogenously injected labeled recombinant αKlotho was detected in the kidney and in urine of rats. Both in vivo (micropuncture) and in vitro (proximal tubule cell line) studies showed that αKlotho traffics from the basal to the apical side of the proximal tubule via transcytosis. Thus, we conclude that the kidney has dual roles in αKlotho homeostasis, producing and releasing αKlotho into the circulation and clearing αKlotho from the blood into the urinary lumen.     

Does Nephrectomy for Trauma Increase the Risk of Renal Failure?

Renal failure is a feared complication following operations for severe trauma. Injuries to the kidney may be managed by nephrectomy or nephrorrhaphy. Nephrectomy may increase the risk of renal failure in already at-risk trauma patients. Nephrectomy for trauma should be avoided to the extent possible because it is associated with renal failure. From a prospectively collected trauma database, 59 patients with nephrectomy were matched at 1:1 ratio with 59 patients with nephrorrhaphy. Matching criteria were age (± 5 years), Injury Severity Score (± 3), abdominal Abbreviated Injury Score (± 1), and mechanism of injury (blunt or penetrating). The rates of renal function compromise (defined as a serum creatinine level >2 mg/dl for more than 2 days) and renal replacement therapy (continuous or intermittent) were compared in the two groups. The two groups were well-matched and similar with regard to injury severity and organs injured. Between nephrectomy and nephrorrhaphy patients, there were no differences in renal function compromise (10% vs. 14%, p = 0.57), renal replacement therapy (5% vs. 0%, p = 0.12), length of hospital stay (19 ± 26 vs. 20 ± 21, p = 0.8), and mortality (15% vs. 12%, p = 0.59). Salvaging the injured kidney does not seem to offer an obvious clinical benefit regarding postoperative renal function. Given the increased operative complexity of nephrorrhaphy in comparison to nephrectomy and the frequent need to abbreviate the operation in patients with severe trauma, nephrectomy should not be avoided when appropriate.     

Renal paratransplant hernia: an unusual complication of renal transplantation?

Renal paratransplant hernia constitutes an unusual variant of internal hernia caused by entrapment of bowel through a defect in the peritoneum covering the transplanted kidney. Only three cases have been previously reported. We present three new cases of renal paratransplant hernia. Abdominal pain and vomiting were the main symptoms. Clinical diagnosis of bowel obstruction and paratransplant hernia was reached using abdominal CT scan. All patients underwent an emergency surgical procedure, and one patient needed resection of necrotic bowel. The three patients survived owing to early surgical intervention, and they were discharged asymptomatic. Paratransplant hernia represented 1.1% of our series of transplant patients. Early diagnosis and surgical treatment are esential in transplant patients with bowel obstruction to avoid high morbidity and mortality rates.     

Treatment of Advanced and Metastatic Renal Cancer: A Revolution?

ContextA significant proportion of patients with renal cell carcinoma (RCC) will experience recurrence or tumour progression after surgical treatment. Nowadays, several treatment options, including immunotherapy and targeted therapies, are available for management of advanced and metastatic RCC.ObjectiveThis paper aims to give an overview of the current treatment options for patients with advanced and metastatic RCC.Evidence acquisitionThis paper is based on a presentation given at the 6th Meeting of the European Society of Oncological Urology 2009, held in Istanbul, Turkey. Data were retrieved from recent review articles, original articles, and abstracts on the treatment of advanced and metastatic RCC.Evidence synthesisThe potential role of adjuvant vaccines in treatment of patients with advanced RCC after nephrectomy has been suggested. With regard to the newly developed targeted agents for treatment of metastatic clear-cell RCC, sunitinib and bevacizumab plus interferon-α (INF-α) seem promising as first-line therapy for good- and intermediate-risk patients. Temsirolimus appears to be effective as first-line treatment in metastatic RCC (mRCC) patients with poor prognosis. Sorafenib and everolimus should be considered as second-line therapy in mRCC patients. Some targeted therapies have also demonstrated clinical activities in patients with metastatic non–clear-cell RCC. Although grade 1 and grade 2 treatment-related adverse events were common with targeted therapies, most were manageable. The effect of targeted agents in earlier stage disease is currently under investigation. Cytokine therapy was associated with a modest survival benefit in mRCC. A combined analysis, however, suggested that cytoreductive nephrectomy might improve survival in patients with mRCC treated with interferon immunotherapy.ConclusionsMore research on the use of adjuvant vaccines in treating patients with advanced RCC is warranted. Although the management of metastatic disease has undergone a revolution in recent years, a lot of questions still need to be answered.     

Renal Cyp3a5-Expressing Genotype Decreases Tacrolimus-to-Dose Ratio in Small Cohort of Renal Transplant Recipients—Preliminary Report

BackgroundPrevious reports have established that patient CYP3A5 allelic variability may be the most important genetic contributor to interindividual variation in tacrolimus exposure in renal transplant recipients. However, CYP3A5 protein is expressed in the allogenic kidney. The aim of this study was to investigate the role of the renal CYP3A5 genotype in tacrolimus concentration-to-dose ratio within 3 years posttransplant.MethodsA retrospective cohort study of 90 renal transplant recipients and their donors evaluated the effect of the CYP3A5 single-nucleotide polymorphism (rs776746) on tacrolimus exposure. The area under the curve for tacrolimus concentration-to-dose ratio within 3-year follow-up was calculated and compared in kidneys carrying at least 1 CYP3A5*1 allele and those carrying the CYP3A5*3/*3 genotype.ResultsA significant effect of CYP3A5 expression on tacrolimus exposure was observed in both donors (mean ± SD: 23.8 ± 7.9 vs 32.6 ± 7.4 ng/mL/mg, respectively; P < .001) and recipients (mean ± SD: 27.1 ± 8.0 vs 32.2 ± 7.9 ng/mL/mg, respectively; P = .034) and was lower when CYP3A5 enzyme occurred. Thus, new groups were formed: the group in which at least 1 of the pairs, donor or recipient, had a CYP3A5 expressing allele (n = 23) had lower exposure to tacrolimus compared with nonexpressors (n = 67; mean ± SD: 26.2 ± 7.6 vs 33.2 ± 7.4 ng/mL/mg, respectively; P < .001).ConclusionIntrarenal metabolism of tacrolimus may affect both local and systemic drug exposure. Nonexpressors receiving kidneys with the CYP3A5*1 allele may benefit from higher tacrolimus doses to hasten achievement of target drug concentrations.     

Renal complications of Castleman’s disease: report of two cases and analysis of 75 cases

Biopsy-proven renal complications of Castleman’s disease (CD) are rare and current knowledge is largely based on sporadic case reports. We reported two more cases, both of which were multicentric CD with hyaline-vascular pathological pattern and presented with chronic renal failure. Case 1 was multicentric CD with renal mesangial proliferative glomerulonephritis complications, and case 2 was multicentric CD with membranoproliferative glomerulonephritis-like complications. Although both were eventually administered corticosteroids combined with cytotoxic drugs, both behaved in an aggressive and relapsing manner. We then made an analysis of 75 cases of biopsy-proven renal complications of CD (including our two cases) which were reported in 51 English literatures from January 1954 to March 2011. We found that the clinical and histological findings of renal complications of CD were heterogeneous. Death was observed in 17% patients after a median follow-up time of 22 months (0–204 months) since histological diagnosis of renal complications. The estimated 5-year cumulative survival rate was 75%. Better understanding and therapeutic interventions are required in further investigations.