Is the renal space closed?

The aim of this study is to verify the aperture or the closure of the renal space. The study is undertaken on histological sections of fetuses in the horizontal and sagittal planes. On each side, the kidney and the suprarenal gland are disposed in a space that is closed on all sides. The anterior and posterior layers of the renal fascia fuse at the upper pole of the space to become continuous with the inferior fascia of the diaphragm. Likewise, they merge at the lower pole and at the lateral border of the space to become continuous with the fasciae of the parietal muscles. At the medial border of the space, the two layers merge to continue medially with the peri-aortocaval connective tissue; they penetrate the hilum and beneath it enclose the ureter.     

Does renal ageing affect survival?

The effects of ageing on progressive deterioration of renal function, both in human and experimental animals, are described elsewhere, but the effect of renal damage on overall survival and longevity is not yet clearly established. The wild-type animals of various genetic backgrounds, fed with regular diet, overtime develop severe age-associated nephropathy, that include but not limited to inflammatory cell infiltration, glomerulosclerosis, and tubulointerstitial fibrosis. Such renal damage significantly reduces their survival. Reducing renal damage, either by caloric restriction or by suppressing growth hormone (GH)/insulin-like growth factor-1 (IGF-1) activity could significantly enhance the longevity of these animals. Available survival studies using experimental animals clearly suggest that kidney pathology is one of the important non-neoplastic lesions that could affect overall survival, and that restoration of renal function by preventing kidney damage could significantly extend longevity. Careful long-term studies are needed to determine the human relevance of these experimental studies.     

Can renal oncocytoma be distinguished from chromophobe renal cell carcinoma by the presence of fibrous capsule?

The most important differential diagnosis of chromophobe renal cell carcinoma (CRCC) is renal oncocytoma. Due to overlapping morphological characteristics of renal oncocytoma and CRCC, particularly its eosinophilic variant, making a correct diagnosis can be challenging. To date, no data are available on the presence of the tumor fibrous capsule as a diagnostic feature in differentiating these tumors. The main purpose of this study was to establish the presence and compare the thickness of the tumor fibrous capsule between two tumor groups. A total of 37 tumors—18 cases of CRCC (three eosinophilic and 15 classic) and 19 cases of renal oncocytoma—were analyzed. Four slides of each tumor stained with hematoxylin and eosin were first scanned at low-power magnification (×40) to assess the presence of the capsule. If present, the capsule was measured in three different thickest areas at higher magnification (×200). The mean value of capsule thickness was calculated and taken into consideration. The capsule was present in 12 (66.7%) cases of CRCCs and in only two (10.5%) cases of renal oncocytomas. Statistical analysis showed significant difference between the presence of fibrous capsule in these two observed tumor groups (P?=?0.001). Average thickness of capsule in CRCCs was 337.7 μm, and 115.4 μm in renal oncocytomas, but the median was not statistically significant (P?=?0.198). Studies with a larger number of cases are needed to conclude if this characteristic could be a low-cost, reliable microscopic feature in differentiating between CRCC and renal oncocytoma.     

Do high-flux dialysis membranes affect renal dyslipidemia?

High-flux hemodialysis has been reported to attenuate renal dyslipidemia. To evaluate the contribution of dialysis membrane composition per se, we compared the impact on the lipoprotein profile of hemodialysis (HD) with a conventional cellulose dialysis membrane with that of a synthetic high-flux dialysis membrane in standard hemodialysis mode. Forty-two patients (24 men, 18 women; mean age, 69 years; range, 39-85 years) on maintenance HD with cellulosic dialysis membranes were randomized and stratified for diabetes mellitus to 12 weeks of HD treatment with either a cellulose acetate (CA; n = 23) or polyacrylonitrile (AN69; n = 19) membrane. HD was performed in a conventional low-flux standard HD mode 4-6 hours/session. Plasma levels of lipids (TC, TG), apolipoproteins (A-I, B, C-III, E), lipoprotein (a) (Ip(a)), and individual apoA and apoB containing lipoproteins (LP-A-I, LP-A-I:A-II, LP-B, LP-Bc) were determined. At baseline, the AN69 group had slightly higher plasma concentrations of apoC-III and C-III/HS, but there were no other differences at entry in study variables between the treatment groups. Twelve week treatment with an AN69 membrane did not result in any significant changes in lipoprotein profile compared with treatment with a cellulose acetate membrane. HD with AN69 dialysis membranes in the conventional low-flux standard hemodialysis mode does not affect the lipoprotein profile.     

Spectrum of renal pathology in adult patients with congenital renal anomalies—a series from a tertiary cancer center

Congenital renal anomalies (CRAs) detected in adults include horseshoe kidney (HK), crossed renal ectopia, and malrotation. Congenital renal anomalies are rare, and renal lesions associated with CRA are rarer. Thirteen patients (11 men and 2 women) were referred to our center with renal masses in the context of CRAs, which included HK (10 cases), crossed renal ectopia (2 cases), and a pelvic kidney (1 case). The mean age at diagnosis was 60 years (37-76 years). All patients were treated with open surgery; 10, partial nephrectomies; 4, radical nephrectomies; and 1, nephroureterectomy with division of the renal isthmus. Pathology ranged from benign (simple cortical cysts, chronic pyelonephritis with secondary hydronephrosis) to malignant (12 cases of renal cell carcinomas [RCCs] and 1 case of urothelial carcinoma). Two patients of HKs presented with bilateral renal masses. The size of the RCC ranged from 2.5 to 13 cm. There were 11 cases of clear cell RCC, 1 case of papillary RCC (type 1), and 1 case of urothelial carcinoma. All the cases of RCC had negative surgical margins. Follow-up available in all patients ranged from 1 month up to 49 months. None of the patients developed any locoregional recurrences or distant metastases. In this patient cohort, the most common congenital anomaly associated with RCC is HK. All tumors behaved in an indolent fashion with prognosis related to pathologic tumor stage. Partial nephrectomy is a safe and effective procedure in appropriately selected patients.     

Pediatric renal cell carcinomas: where do they fit in the new histologic classification of renal cell carcinoma?

Genetic, immunohistochemical, and histologic data has led to the reclassification of renal cell carcinoma in the last decade. Recent studies suggest that renal cell carcinomas in children and young adults may represent a distinct group of tumors. These tumors have unique genetic findings (most commonly t(x;1)(p11:q21)), a predominantly papillary architecture, numerous calcifications, granular cytoplasm, and a possible relationship with neuroblastoma.     

Identification and characterization of Birt-Hogg-Dubé associated renal carcinoma

The Birt-Hogg-Dubé (BHD) gene is responsible for BHD syndrome, a rare autosomal dominant disease, characterized by benign hair follicle tumours, spontaneous pneumothorax and renal neoplasms with diverse histology. To elucidate its involvement in the development of renal neoplasms, we examined a total of 100 sporadic renal tumours with various histological subtypes for BHD mutation by SSCP-sequencing analyses. We found one germline insertion mutation in the C8 hotspot of exon 11 (c.1733insC), which is known to have a strong association with renal tumour occurrence. The germline-mutated patient suffered from solitary renal cell carcinoma (RCC) but did not have any other BHD manifestations or family history. The tumour revealed heterogeneous cytomorphology, mainly a mixture of eosinophilic and focally clear cells with tubulopapillary architecture. In this tumour, both BHD alleles were inactivated by germline mutation concomitant with loss of heterozygosity, and the amount of BHD mRNA detected by real-time quantitative PCR (RQ-PCR) was very low. Renal tumour subtype/nephron segment-specific gene expression detected by RQ-PCR demonstrated that the tumour expressed relatively high amounts of alpha-methylacyl-CoA racemase (AMACR) and the KIT oncogene, but relatively low amounts of carbonic anhydrase IX (CA9), aquaporin 1 (AQP1), claudin 7 (CLDN7), parvalbumin (PVALB), chloride channel Kb (CLCNKB) and 11-beta-hydroxysteroid dehydrogenase 2 (HSD11B2), suggesting diverse mRNA signatures. Further clustering analysis of 88 renal tumours based on expression of these eight genes sub-classified the tumour as close to oncocytomas and chromophobe RCCs, which are considered distal nephron-associated tumours. These data suggest that somatic mutation of BHD is relatively rare in Japanese patients. The BHD-mutated RCC identified in this study, which exhibits heterogeneous biological features in both morphology and gene expression signatures, seems to deviate from our current understanding of renal tumour classification.     

Are renal microgranulomas related to inflammatory tubular destruction?

Two cases of renal microgranuloma formation are reported, one in a patient with known Crohn's disease and another in a case of acute renal allograft rejection. In both cases, the microgranulomas arose as a result of inflammatory tubular destruction, in a manner analogous to that seen in patients with ulcerative colitis arising adjacent to ruptured epithelial crypts in the large intestine. Microgranulomas may occur at multiple anatomical sites in Crohn's disease, although renal microgranulomas are very rare. Non-specific inflammatory tubular destruction should be considered as a cause of renal microgranuloma formation, in addition to systemic granulomatous diseases, such as tuberculosis, sarcoid, or Crohn's disease, when granulomas are seen in the presence of inflammatory tubular destruction in renal biopsies.     

Effect of the IABP on the renal artery bloodflow

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Are gadolinium-based contrast media nephrotoxic? A renal biopsy study

Gadolinium-based contrast media were originally introduced as alternatives to iodinated media for magnetic resonance imaging. Although originally thought to be nonnephrotoxic, gadolinium-based contrast media have recently been reported to be associated with acute renal failure; the mechanism and the underlying renal injury are not completely understood. We report what is, to our knowledge, the first renal biopsy in this context. A 56-year-old patient underwent 2 consecutive vascular imaging procedures in conjunction with gadolinium-based contrast medium administration. A few days later, the patient developed acute renal failure. A renal biopsy showed acute tubular cell injury including patchy tubular cell necrosis, tubular cell degeneration, and marked proliferation of tubular cells, together with mild interstitial edema and interstitial inflammation, but without significant glomerular or vascular changes. During supportive therapy, renal function was partially regained. This case emphasizes the potential nephrotoxicity of gadolinium-based contrast media and suggests that the nephrotoxicity is related to potentially reversible acute tubular cell injury.     

Dialysis in acute renal failure: is more better?

An increasing body of evidence indicates therapy dose and intensity influence the outcome of dialyzed ARF patients. However, a number of unanswered questions remain on this issue. These questions need to be addressed in future prospective, controlled trials that assess the effect of dose and intensity on outcome both within and between the various ARF renal replacement therapies, with appropriate and clinically relevant control arms. Such investigations should provide guidelines ultimately for the dialytic management of critically ill patients with ARF.     

Is bradykinin a mediator of renal neuropeptide Y effects?

We have previously reported that the bradykinin receptor antagonist icatibant attenuates the neuropeptide-Y-induced diuresis and natriuresis in anaesthetized rats (Am J Physiol 275:F502-F509, 1998). Therefore, we have now determined whether bradykinin mimics tubular responses to neuropeptide Y in acutely pentobarbital-anaesthetized rats. Infusion of the neuropeptide Y receptor agonist peptide YY (2 micrograms kg-1 min-1) enhanced diuresis and natriuresis approximately equal to 2- and 4-fold, respectively, but did not increase urinary bradykinin excretion. Intrarenal infusion of bradykinin (100 ng kg-1 min-1) reduced renal blood flow by approximately equal to 12% and this was abolished by concomitant administration of icatibant (200 ng kg-1 min-1). However, intrarenal bradykinin infusion did not affect creatinine clearance, urine flow rate or sodium excretion (basal values: 0.8 ml min-1, 111 microliters/15 min and 7.7 mumol/15 min, respectively). These data do not support our original hypothesis that bradykinin mediates the renal effects of neuropeptide Y.