Results of Nephrectomy in Hypertension Associated with Unilateral Renal Disease

Nephrectomy has been carried out in 34 patients with hypertension associated with unilateral parenchymal renal disease (28 with unilateral pyelonephritis, 3 tuberculosis, 2 hypoplasia, and 1 adenocarcinoma). In 13 of the patients the blood pressure was corrected, in four it was improved, and in 17 it was unaffected. The intravenous pyelogram (by the infusion technique with nephrotomography if necessary) and renogram give adequate information in most patients with unilateral parenchymal renal disease but may need to be supplemented by aortography, or retrograde pyelography, or divided renal function studies in a few special circumstances. When the function of the damaged kidney is less than 25% of the total (which is well maintained), and the contralateral kidney is intact, nephrectomy is recommended provided the hypertension is significant; success is more likely in younger patients with a short history of hypertension.     

Peritoneal Dialysis in Chronic Renal Failure

The long-term results of intermittent peritoneal dialysis in long-term treatment of renal disease have yet to equal those of intermittent hemodialysis. However, further exploration and refinement of this technique is justified.Performed in acute stages of disease, both peritoneal dialysis and hemodialysis relieve the symptoms of uremia and specifically “buy time” for the patient so that proper medical or surgical therapy may be instituted. In acute situations, peritoneal dialysis is the procedure of choice, and is an important adjunct to more conventional treatment for chronic renal disease. It may be useful sometimes even in chronically hemodialyzed patients—for example, when the hemodialysis cannula for one reason or another is inaccessible because of clots, replacement, or infection. It is especially valuable when the hemorrhagic complications of uremia contraindicate hemodialysis treatment.Its use in chronic uremia remains sharply limited in time, but for brief periods chronic peritoneal dialysis appears to be a reasonably satisfactory means of prolonging life while awaiting homotransplant or decision for maintenance hemodialysis therapy.     

Hemorrhagic Fever with Renal Syndrome Complicated by Orchitis

Hemorrhagic fever with renal syndrome (HFRS) is a disease caused by viruses of the family Bunyaviridae,genus Hantavirus.HFRS from Dobrava virus (DOBV) is a seldom reported disease in Albania.Clinically HFRS is manifested as mild,moderate,or severe.Therefore,the number of cases of Hantavirus' infection may be underestimated,and should be included in the differential diagnosis of many acute infections,hematologic diseases,acute abdominal diseases and renal diseases complicated by acute renal failure.We report...     

The Renal Arterial Resistive Index and Stage of Chronic Kidney Disease in Patients with Renal Allograft

Objective

The study investigated the optimal threshold value of renal arterial resistive index as assessed by Doppler ultrasonography determining chronic kidney disease stage 4 or higher in patients with renal allograft.

Methods

In a cross-sectional study the renal arterial resistive index were obtained in interlobar arteries by Doppler ultrasonography in 78 patients with renal allograft. The stage of chronic kidney disease was determined by the estimated glomerular filtration rate equation.

Results

The median renal arterial resistive index was 0.61 (interquartile range, 0.56 to 0.66). We observed a significant association between renal arterial resistive index above the upper quartile and chronic kidney disease stage 4 or higher (relative risk, 4.64; 95% confidence interval, 1.71 to 12.55; p = 0.003 by Fisher’s exact test). Multivariate logistic regression analysis showed that renal arterial resistive indices (p = 0.02) and time since transplantation (p = 0.04), but not age, gender, or blood pressure were significantly associated with chronic kidney disease stage 4 or higher.

Conclusion

A renal arterial resistive index higher than 0.66 may determine the threshold value of chronic kidney disease stage 4 or higher in patients with renal allograft.     

Differential Renal Function Studies in the Diagnosis of Renal Hypertension

Over a 10-year period, positive criteria of the Howard test and the Rapoport Index have shown consistently good correlation with sustained relief or marked improvement in hypertension, in patients with main renal artery lesions. Similar correlation was obtained with ischemic criteria from histopathologic studies.Differential function studies did not reveal positive ischemic criteria in any patient operated upon for unilateral parenchymal disease. Histopathologic criteria of ischemia were also infrequent in this group. Nevertheless, marked improvement or cure of hypertension occurred in 62% of the latter. No factor can be used to predict improvement in this type of renal hypertension. Differential renal function criteria may occasionally appear to indicate renal artery ischemia in the more normal kidney in patients with unilateral parenchymal renal disease; wrong interpretation is avoided by taking differential creatinine clearance into account. Until vasopressor substances can be easily measured and accurately interpreted, aortography is indicated in selected patients.     

Renal organogenesis

The increasing prevalence of chronic kidney disease in the absence of new treatment modalities has become a strong driver for innovation in nephrology. An increasing understanding of stem cell biology has kindled the prospects of regenerative options for kidney disease. However, the kidney itself is not a regenerative organ, as all the nephrons are formed during embryonic development. Here, we will investigate advances in the molecular genetics of renal organogenesis, including what this can tell us about lineage relationships, and discuss how this may serve to inform us about both the normal processes of renal repair and options for regenerative therapies.     

Renal denervation: a new treatment option in resistant arterial hypertension

Hypertension is one of the most prevalent cardiovascular risk factors. Despite this high prevalence and a broad availability of effective pharmaceutical agents, a significant proportion of patients do not reach treatment goals. Partly this can be explained by secondary causes of hypertension or non-compliance of patients. Nevertheless, a subgroup of patients can be diagnosed with ‘resistant hypertension’. Activation of the sympathetic nervous system is known to be an important factor in the development and progression of systemic hypertension. In this context, a percutaneous, catheter–based approach has been developed using radiofrequency energy to disrupt renal sympathetic nerves. The first studies have shown this technique to be safe, illustrated by a lack of vascular or renal injury. More importantly, catheter-based renal nerve ablation resulted in a significant reduction in blood pressure on top of traditional medical therapy. Additional to the encouraging effects shown on hypertension, a positive influence of this intervention in other conditions, characterised by sympathetic overactivation, may be expected. Though this technique seems promising, further studies are needed to address long-term safety and efficacy of renal denervation in hypertension and other disease states.     

Renal Expression of FGF23 in Progressive Renal Disease of Diabetes and the Effect of Ace Inhibitor

Fibroblast growth factor 23 (FGF23) is a phosphaturic hormone mainly produced by bone that acts in the kidney through FGF receptors and Klotho. Here we investigated whether the kidney was an additional source of FGF23 during renal disease using a model of type 2 diabetic nephropathy. Renal expression of FGF23 and Klotho was assessed in Zucker diabetic fatty (ZDF) and control lean rats at 2, 4, 6, 8 months of age. To evaluate whether the renoprotective effect of angiotensin converting enzyme (ACE) inhibitor in this model was associated with changes in FGF23 and Klotho, ZDF rats received ramipril from 4, when proteinuric, to 8 months of age. FGF23 mRNA was not detectable in the kidney of lean rats, nor of ZDF rats at 2 months of age. FGF23 became measurable in the kidney of diabetic rats at 4 months and significantly increased thereafter. FGF23 protein localized in proximal and distal tubules. Renal Klotho mRNA and protein decreased during time in ZDF rats. As renal disease progressed, serum phosphate levels increased in parallel with decline of fractional phosphorus excretion. Ramipril limited proteinuria and renal injury, attenuated renal FGF23 upregulation and ameliorated Klotho expression. Ramipril normalized serum phosphate levels and tended to increase fractional phosphorus excretion. These data indicate that during progressive renal disease the kidney is a site of FGF23 production which is limited by ACE inhibition. Interfering pharmacologically with the delicate balance of FGF23 and phosphorus in diabetes may have implications in clinics.     

Renal tubular acidosis: developments in our understanding of the molecular basis

Renal tubular acidosis is a metabolic acidosis due to impaired acid excretion by the kidney. Hyperchloraemic acidosis with a normal anion gap and normal (or near normal) glomerular filtration rate, and in the absence of diarrhoea, defines this disorder. However, systemic acidosis is not always evident and renal tubular acidosis can present with hypokalaemia, medullary nephrocalcinosis and recurrent calcium phosphate stone disease, as well as growth retardation and rickets in children, or short stature and osteomalacia in adults. Renal dysfunction in renal tubular acidosis is not always confined to acid excretion and can be part of a more generalised renal tubule defect, as in the renal Fanconi syndrome. Isolated renal tubular acidosis is more usually acquired, due to drugs, autoimmune disease, post-obstructive uropathy or any cause of medullary nephrocalcinosis. Less commonly, it is inherited and may be associated with deafness, osteopetrosis or ocular abnormalities. The clinical classification of renal tubular acidosis has been correlated with our current physiological model of how the nephron excretes acid, and this has facilitated genetic studies that have identified mutations in several genes encoding acid and base ion transporters. In vitro functional studies of these mutant proteins in cell expression systems have helped to elucidate the molecular mechanisms underlying renal tubular acidosis, which ultimately may lead to new therapeutic options in what is still treatment only by giving an oral alkali.     

Renal Involvement in Non-Hodgkin Lymphoma: Proven by Renal Biopsy

Aims

To determine the spectrum of renal lesions in patients with kidney involvement in non-Hodgkin''s lymphoma (NHL) by renal biopsy.

Methods

The clinical features and histological findings at the time of the renal biopsy were assessed for each patient.

Results

We identified 20 patients with NHL and renal involvement, and the diagnosis of NHL was established following the kidney biopsy in 18 (90%) patients. The types of NHL include the following: chronic lymphocytic leukemia/small lymphocytic lymphoma (n = 8), diffuse large B-cell lymphoma (n = 4), T/NK cell lymphoma (n = 3), lymphoplasmacytic lymphoma (n = 2), cutaneous T-cell lymphoma (n = 1), mucosa-associated lymphoid tissue lymphoma (n = 1) and mantle cell lymphoma (n = 1). All presented with proteinuria, and 15 patients had impaired renal function. The pathological findings included (1) membranoproliferative glomerulonephritis-like pattern in seven patients; (2) crescent glomerulonephritis in four; (3) minimal-change disease in three, and glomeruli without specific pathological abnormalities in three; (4) intraglomerular large B-cell lymphoma in one; (5) intracapillary monoclonal IgM deposits in one; (6) primary diffuse large B-cell lymphoma of the kidneys in one; and (7) lymphoma infiltration of the kidney in eight patients.

Conclusion

A wide spectrum of renal lesions can be observed in patients with NHL, and NHL may be first proven by renal biopsies for evaluation of kidney injury or proteinuria. Renal biopsy is necessary to establish the underlying cause of renal involvement in NHL.     

The Function of MicroRNAs in Renal Development and Pathophysiology

MicroRNAs (miRNAs) are a class of endogenous small non-coding RNAs that modulate diverse biological processes predominantly by translation inhibition or induction of mRNA degradation. They are important regulatory elements involved in renal physiology and pathology. Dysregulation of miRNAs disrupts early kidney development, renal progenitor cell differentiation and the maintenance of mature nephrons. miRNAs are also reported to participate in various renal diseases, including chronic kidney disease, acute kidney injury, allograft acute rejection and renal cell carcinoma. Differentially regulated miRNAs may represent innovative biomarkers for diagnosis and prognosis. Therefore, determining the roles of miRNAs in different types of renal diseases will help to clarify the pathogenesis and facilitate the development of novel therapies.     

肾癌预后分子生物标记物研究进展

肾癌发病率约占全身恶性肿瘤的3%。肾癌组织学行为多变,预后有不确定性。外科手术可以治疗局限性肾癌,但有将近20%的局限性肾癌患者原发肿瘤切除后出现转移,而且肾癌对化疗及放疗均不敏感。基于此临床上开展了许多辅助试验的研究,并建立了许多模型来研究肾癌术后的预后,而模型的精准度一般都需要依据肾癌的生物标记物监测。有很多分子生物标记物已经证实和肾癌预后相关,如VHL、P53、Ki-67等,本文综述了肾癌预后的分子生物标记物的最新进展。     

Association of Dyslipidemia with Renal Outcomes in Chronic Kidney Disease

Dyslipidemia is highly prevalent in patients with chronic kidney disease (CKD) and the relationship between dyslipidemia with renal outcomes in patients with moderate to advanced CKD remains controversial. Hence, our objective is to determine whether dyslipidemia is independently associated with rapid renal progression and progression to renal replacement therapy (RRT) in CKD patients. The study analyzed the association between lipid profile, RRT, and rapid renal progression (estimated glomerular filtration rate [eGFR] slope <−6 ml/min/1.73 m²/yr) in 3303 patients with stages 3 to 5 CKD. During a median 2.8-year follow-up, 1080 (32.3%) participants commenced RRT and 841 (25.5%) had rapid renal progression. In the adjusted models, the lowest quintile (hazard ratios [HR], 1.23; 95% confidence interval [CI], 1.01 to 1.49) and the highest two quintiles of total cholesterol (HR, 1.25; 95% CI, 1.02 to 1.52 and HR, 1.35; 95% CI, 1.11 to 1.65 respectively) increased risks for RRT (vs. quintile 2). Besides, the highest quintile of total cholesterol was independently associated with rapid renal progression (odds ratio, 1.36; 95% CI, 1.01 to 1.83). Our study demonstrated that certain levels of dyslipidemia were independently associated with RRT and rapid renal progression in CKD stage 3–5. Assessment of lipid profile may help identify high risk groups with adverse renal outcomes.     

Tubulocystic Renal Cell Carcinoma: A Great Imitator

Tubulocystic renal cell carcinoma (TCRC) is a rare renal tumor. Patients are usually asymptomatic; it is usually detected incidentally, during imaging studies for Bosniak type III and type IV renal cysts. These tumors rarely metastasize. The role of targeted therapy in such rare tumors is still controversial. We report a case of TCRC initially presented as a Bosniak type II renal cyst and was discovered ultimately to be a metastatic disease. This type of presentation might broaden our understanding of this rare disease.     

Lipoprotein X Causes Renal Disease in LCAT Deficiency

Human familial lecithin:cholesterol acyltransferase (LCAT) deficiency (FLD) is characterized by low HDL, accumulation of an abnormal cholesterol-rich multilamellar particle called lipoprotein-X (LpX) in plasma, and renal disease. The aim of our study was to determine if LpX is nephrotoxic and to gain insight into the pathogenesis of FLD renal disease. We administered a synthetic LpX, nearly identical to endogenous LpX in its physical, chemical and biologic characteristics, to wild-type and Lcat^-/- mice. Our in vitro and in vivo studies demonstrated an apoA-I and LCAT-dependent pathway for LpX conversion to HDL-like particles, which likely mediates normal plasma clearance of LpX. Plasma clearance of exogenous LpX was markedly delayed in Lcat^-/- mice, which have low HDL, but only minimal amounts of endogenous LpX and do not spontaneously develop renal disease. Chronically administered exogenous LpX deposited in all renal glomerular cellular and matrical compartments of Lcat^-/- mice, and induced proteinuria and nephrotoxic gene changes, as well as all of the hallmarks of FLD renal disease as assessed by histological, TEM, and SEM analyses. Extensive in vivo EM studies revealed LpX uptake by macropinocytosis into mouse glomerular endothelial cells, podocytes, and mesangial cells and delivery to lysosomes where it was degraded. Endocytosed LpX appeared to be degraded by both human podocyte and mesangial cell lysosomal PLA₂ and induced podocyte secretion of pro-inflammatory IL-6 in vitro and renal Cxl10 expression in Lcat^-/- mice. In conclusion, LpX is a nephrotoxic particle that in the absence of Lcat induces all of the histological and functional hallmarks of FLD and hence may serve as a biomarker for monitoring recombinant LCAT therapy. In addition, our studies suggest that LpX-induced loss of endothelial barrier function and release of cytokines by renal glomerular cells likely plays a role in the initiation and progression of FLD nephrosis.     

Renal disease,epidermal necrosis,and epithelial cell antibodies.

OBJECTIVE--To describe the association between epithelial cell IgM, which has previously been associated with an increased incidence of loss of renal graft in children, with a novel cutaneous eruption and unexplained native renal disease. DESIGN--Observational study on children with epithelial cell antibody presenting with unexplained renal or skin disease. SETTING--General paediatric department and regional paediatric nephrology unit. PATIENTS--Six children (five girls, one boy), who presented to the unit in 1989-90. RESULTS--Three children, two of whom had a history of a hyperpigmented rash, presented with hypertension, proteinuria, and impaired renal function. Renal biopsy specimens from two of these children showed severe arteriolar endothelial cell swelling with arteriolar occlusion. These children fully recovered after treatment with antihypertensive drugs. The third child developed end stage renal failure and required dialysis. Three other children presented with an unusual cutaneous eruption but no evidence of renal disease. Histology of the skin lesions showed acute epidermal necrosis and features consistent with a viral infection. CONCLUSIONS--The aetiology and pathogenesis of the epithelial cell antibody are unknown. These cases indicate that it may have a role in native kidney disease and focal epidermal necrosis. Clinical and histological features suggest that the antibody may be associated with a viral infection.     

Late Failure in Cadaveric Renal Allografts

Sixteen patients with renal cadaveric allografts who have survived for one year or longer are reported. The patients were analyzed from the standpoint of incidence, quantity and course of proteinuria in relation to renal function and the nature of the original disease.This analysis shows that proteinuria is progressive and is accompanied by a decline in renal function when the original disease is of an immune nature. This was not so in patients with non-immune original disease. These findings suggest that recurrence of original disease plays an important role in late failure of cadaveric renal allografts.     

Diagnosis and Surgical Treatment of Renal Hydatid Disease: a Retrospective Analysis of 30 Cases

Echinococcosis (CE) is an infection which is caused by the larval stage of a tapeworm and is endemic in stockbreeding regions of developing countries. The kidney is the most commonly affected organ in the urinary tract. However, reports on renal hydatid disease are limited in the literature, and usually there are no specific clinical characteristics and promising operative methods. The purpose of this study is to assess the most appropriate surgical technique for the patient with urinary tract CE. We retrospectively analyzed thirty patients with renal hydatid cysts who received different surgical treatments in the urology department of the First Affiliated Hospital of Xinjiang Medical University from February 1985 to April 2010. Twenty patients were males and ten were females. The diagnostic accuracy was 74%, 87.5%, and 66.6% respectively by using of ultrasound, CT, and laboratory tests. Thirty patients were followed up for 1–15 years after surgery. One patient experienced a recurrence of renal CE. The ultrasound, CT, and immunological tests are an important means of diagnosis. The surgical treatment principle of renal hydatid should be based on residual renal function, hydatid cyst size, number, location, and surgical techniques to determine the surgical plan to retain the renal function.