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PubMed1991

Seminal vesicle cysts: association with adult polycystic kidney disease.

Adult polycystic kidney disease (APKD) is associated with cyst formation in the kidney, liver, pancreas, esophagus, ovary, uterus, and brain. Four patients with APKD (aged 45-65 years) with computed tomographic evidence of seminal vesicle cysts are described. All seminal vesicles contained cystic masses with attenuation values of 0-30 HU. Seminal vesicle thickness was 3-4 cm (normal, 1.5 cm). High-attenuation walls separated the cysts, which were 3-35 mm in diameter. All patients had typical renal stigmata of APKD. None had cysts elsewhere, except one patient with hepatic cysts. Postmortem examination in one patient confirmed the seminal vesicle cysts as well as APKD. It is likely that a basement membrane defect allows cyst formation in multiple organs, presumably including the seminal vesicles. Because of the association of seminal vesicle cysts with ipsilateral urogenital anomalies, and because only 60% of patients with APKD have a relevant familial history, the kidneys of patients with cross-sectional imaging evidence of seminal vesicle cysts should also be studied.

Cysts↗
PubMed2001

Current advances in molecular genetics of autosomal-dominant polycystic kidney disease.

Autosomal-dominant polycystic kidney disease results from at least two causal genes, PKD1 and PKD2. The identical clinical phenotype in human patients and targeted Pkd1 and Pkd2 mutant mouse models provides evidence that both gene products act in the same pathogenic pathway. The discovery of direct PKD1 and PKD2 interactions implies that both gene products, polycystin-1 and polycystin-2, play a functional role in the same molecular complex. The spectrum of germ-line mutations in both genes and the somatic mutations identified from individual PKD1 or PKD2 cysts indicate that loss of function of either PKD1 or PKD2 is the mechanism of cystogenesis in autosomal-dominant polycystic kidney disease. A novel mouse model, Pkd2WS25/-, has proved that loss of heterozygosity is the molecular mechanism of autosomal-dominant polycystic kidney disease. Recently, studies on the expression patterns of PKD1 and PKD2 in humans or mice indicate that polycystin 1 and polycystin 2 seem to have their own respective functional roles, even though most of the functions of these polycystins are parallel during human and mouse development. Pkd2-deficient mice have cardiac septum defects, but Pkd1 knockout mice do not have this phenotype. On the other hand, Pkd2 has a very low level of expression in the central nervous system when compared with Pkd1. In addition, the level of expression of Pkd1 is increased during mesenchymal condensation, whereas Pkd2 expression is unchanged. Preliminary data have shown that the PKD1/PKD2 compound trans-heterozygous has a more severe cystic phenotype in the kidney than that of an age-matched heterozygous type 1 or type 2 of autosomal-dominant polycystic kidney disease alone. This finding suggests that PKD1 may be a modifier of disease severity for PKD2, and vice versa. The characteristics of the contiguous PKD1/TSC2 syndrome phenotypes and the data from Krd mice imply that TSC2 and PAX2 may also serve as potential modifiers for the disease severity of autosomal-dominant polycystic kidney disease.

Animals↗
PubMed2005

[Peritoneal dialysis in patients with polycystic kidney disease].

In Austria, patients with end-stage renal disease caused by polycystic kidney disease are less frequently treated with peritoneal dialysis (PD) than patients with noncystic renal diseases (6% versus 8%). In contrast, the United States renal data system reports that more than one fifth of patients with polycystic kidney disease choose PD as their initial form of renal replacement therapy. The reasons for this difference are unknown. Extrarenal manifestations of the disease, such as diverticulosis, development of hernias or vascular aneurysms, may theoretically promote the occurrence of complications typically related to PD. However, studies undertaken to clarify these questions did not find any difference in the rates of peritonitis caused by diverticulosis or Gram-negative bacteria, and no differences were seen with respect to vascular complications. Nevertheless, in comparison with the general population, patients with polycystic kidney disease are more likely to develop hernias, and the incidence of herniation may be further increased by PD. In conclusion, patients with polycystic kidney disease who also have abdominal complaints such as meteorism and discomfort, or lumbago resulting from the markedly enlarged kidneys, should not be actively advised to have PD treatment. The same is true for patients with recurrent hernias. However, the technical survival, quality of dialysis, duration of therapy and rates of complications in PD are comparable in patients with cystic or noncystic kidney disease, and therefore all patients with polycystic kidney disease who do not have abdominal complaints or history of recurrent hernias should be informed that PD is an adequate form of renal replacement therapy, equally effective as hemodialysis.

Austria↗
PubMed2003

Relationship between C-reactive protein, albumin, and cardiovascular disease in patients with chronic kidney disease.

BACKGROUND: C-Reactive protein (CRP) level is elevated in kidney failure and may be related to malnutrition and cardiovascular disease (CVD). Data are limited regarding relationships between CRP levels and glomerular filtration rate (GFR), nutritional indices, and CVD in patients with earlier stages of kidney disease. METHODS: CRP was assayed from samples from the Modification of Diet in Renal Disease (MDRD) Study (n = 801). CRP distributions were compared between the MDRD Study and National Health and Nutrition Examination Survey (NHANES; 1999 to 2000). Associations between CRP level and GFR, nutritional indices, serum albumin levels, and CVD risk factors were examined in the MDRD Study. RESULTS: Geometric means of CRP, adjusted for age and sex, were similar in NHANES (0.23 mg/dL) and the MDRD Study (0.22 mg/dL). In the MDRD Study, CRP level was related directly to measures of body fat and CVD risk factors, inversely with serum albumin level and energy intake, and unrelated to GFR. In multivariable analysis adjusting for other determinants of serum albumin level, high CRP level (>0.6 mg/dL) was associated with a 0.07-g/dL (0.7-g/L; 95% confidence interval [CI], 0.03 to 0.12) lower mean serum albumin level. After adjusting for traditional CVD risk factors, the odds of CVD were 1.73 (95% CI, 1.07 to 2.78) times greater in subjects with a high CRP level. CONCLUSION: GFR level does not appear to influence CRP level in the earlier stages of chronic kidney disease. CRP levels are independently associated with serum albumin level and CVD prevalence. Inflammation may be involved in the pathophysiological state of malnutrition and CVD in the earlier stages of predominantly nondiabetic kidney disease.

Adolescent↗
PubMed1993

Renal stone disease in autosomal dominant polycystic kidney disease.

Nephrolithiasis is an important manifestation of autosomal dominant polycystic kidney disease (ADPKD), which occurs in approximately 20% of patients. It should always enter the differential diagnosis of flank pain in patients with ADPKD. The diagnosis is hindered by the distorted anatomy of the polycystic kidneys and the frequent occurrence of parenchymal and cyst wall calcifications, and requires demonstration of the relationship to the collecting system by intravenous urography and/or computed tomography. Computed tomography is the most sensitive imaging technique for detection of stones or calcifications, whereas intravenous urography is the most sensitive for visualization of the intrarenal collecting system. Precaliceal tubular ectasia can be detected in 15% of patients with ADPKD and nephrolithiasis, but this association may not be specific to ADPKD. The composition of the stones is most frequently uric acid and/or calcium oxalate. Metabolic factors are important in their pathogenesis. Distal acidification defects may be important in a few patients, while an abnormal transport of ammonium, low urine pH, and hypocitruria are the most common abnormalities. The treatment of nephrolithiasis in patients with ADPKD is not different from that in patients without ADPKD. Extracorporeal shock wave lithotripsy and percutaneous nephrostolithotomy in patients with early disease and normal renal function are not contraindicated.

Adult↗
PubMed2005

Arterial compliance in elderly men with chronic kidney disease.

BACKGROUND/AIM: Chronic kidney disease (CKD) is associated with decreased arterial compliance (AC). The stage of development of impaired arterial function in CKD in relation to loss of glomerular filtration rate (GFR) is not known. This study's aim was to evaluate the relationship between GFR and AC in patients with CKD. METHODS: We recruited 91 men aged > or =60 years with GFR 15-89 ml/min (mean 47 +/- 21) to evaluate the relationship between GFR and AC in a cross-sectional study. We measured AC at the brachial artery with an oscillometric device (brachial artery distensibility; BAD). RESULTS: There was no correlation between GFR and BAD (r = 0.08, p = 0.44). When stratified according to CKD stages, all groups showed decreased BAD compared with reference values, and there were no differences among them (one-way ANOVA). Bivariate analyses showed statistically significant correlations between BAD and age (r = -0.23, p = 0.03), antihypertensive drug number (r = 0.27, p = 0.009) and serum hemoglobin (r = 0.24, p = 0.02), but only age and antihypertensive drug number remained significant markers of BAD in a multiple regression model. CONCLUSION: Older men with CKD have impaired arterial function, but GFR and CKD stage have no relationship to the degree of decrease in brachial artery distensibility.

Aging↗
PubMed2005

Liver disease in autosomal recessive polycystic kidney disease.

Hepatic complications occur in a significant proportion of children with autosomal recessive polycystic kidney disease (ARPKD). PKHD1/fibrocystin, the defective gene in ARPKD, is expressed in the cilia of bile duct epithelium and leads to abnormalities in the rubric of the ductal plate malformation. Portal hypertension and biliary disease are the major liver problems seen in ARPKD. Complete blood counting, physical examination, ultrasonography and magnetic resonance (MR) cholangiography are indicated as screening procedures for hepatic disease in ARPKD. Medical and surgical interventions are potentially indicated for children with portal hypertension and/or biliary disease. A high index of suspicion for the diagnosis of cholangitis needs to be maintained in children with biliary disease. The implications of hepatic disease need to be considered in the decision-making regarding renal transplantation in ARPKD.

Biliary Tract Diseases↗
PubMed2004

The involvement of growth hormone (GH), insulin-like growth factors (IGFs) and vascular endothelial growth factor (VEGF) in diabetic kidney disease.

At present, diabetic kidney disease affects about 15-25 % of patients with type 1 diabetes (T1D) and 30-40 % of patients with type 2 diabetes (T2D). Several decades of extensive research have elucidated various pathways to be implicated in the development of diabetic kidney disease. These include metabolic factors beyond blood glucose (e.g. advanced glycation endproducts (AGEs)), haemodynamic factors (e.g. the renin angiotensin system (RAS)), intracellular signaling molecule proteins (e.g. protein kinase C (PKC)) and growth factors/cytokines (e.g. growth hormone (GH), insulin-like growth factors (IGFs), transforming growth factor beta (TGF-beta) and vascular endothelial growth factor (VEGF)). This review focuses on the role of three of these growth factors, i.e. GH, IGFs and VEGF. A brief discussion of each system is followed by description of its expression in the normal kidney. Then, for each system, in vitro, experimental and clinical evidence addressing the role of the system in diabetic kidney disease is presented. The interplay of each system to other potential pathways will also be addressed. Finally, well-known and potential therapeutic strategies targeting the GH/IGF and VEGF systems in a specific or indirect way will discussed.

Animals↗
PubMed1998

Expression of transforming growth factor alpha and epidermal growth factor receptor in adult polycystic kidney disease.

Adult polycystic kidney disease (APKD) is a common genetic disease with a frequency of 1:1000. Evidence suggests that transforming growth factor alpha (TGF alpha) signaling may contribute to the hyperproliferation of the cystic epithelia in APKD. TGF alpha and epidermal growth factor (EGF) are well known mitogens expressed in the kidney and both exert their biological activities through binding to the same EGF receptor. A transgenic mouse that over-expressed TGF alpha developed renal cysts; raised levels of TGF alpha and EGF receptor mRNA were found in kidneys from two autosomal dominant APKD patients. To study the role of TGF alpha in cyst formation, we analyzed nine anatomically diagnosed adult polycystic kidneys and four normal kidneys using immunohistochemistry. We also traced the possible origins of the cysts by staining with the proximal convoluted tubule (PCT) marker, gp330, and the distal convoluted tubule (DCT) and collecting tubule (CT) marker, peanut agglutinin (PNA). In normal kidneys, TGF alpha protein was concentrated in the DCT and CT and EGF receptor protein in all three tubule types. In the early cysts of APKD, the cystic epithelia showed strong positive staining with TGF alpha, EGF receptor and gp330 but negative with PNA. Strong TGF alpha and EGF receptor staining was also found in the mixture of advanced cysts in the end-stage cystic kidneys although the cysts are likely to be derived from different segment of the renal tubules. This increased TGF alpha and EGF receptor expression in all cases and all types of cysts suggests that autocrine/paracrine stimulation by TGF alpha may be a common mechanism in cyst development in APKD.

Adult↗
PubMed1986

[Bacterial kidney disease in salmonids].

Bacterial kidney disease (BKD) is the most important bacterial infection in salmonid fish. Clinics, pathomorphology, distribution and possibility of therapy of BKD are discussed regarding results of literature as well as own experiences.

Animals↗
PubMed2024

Evidence for a relationship between genetic polymorphisms of the L-DOPA transporter LAT2/4F2hc and risk of hypertension in the context of chronic kidney disease.

BACKGROUND: Chronic kidney disease (CKD) and hypertension are chronic diseases affecting a large portion of the population frequently coexistent and interdependent. The inability to produce/use adequate renal dopamine may contribute to the development of hypertension and renal dysfunction. The heterodimeric amino acid transporter LAT2/4F2hc (SLC7A8/SLC3A2 genes) promotes the uptake of L-DOPA, the natural precursor of dopamine. We examined the plausibility that SLC7A8/SLC3A2 gene polymorphisms may contribute to hypertensive CKD by affecting the L-DOPA uptake. METHODS: 421 subjects (203 men and 218 women, mean age of 78.9&#x2009;&#xb1;&#x2009;9.6&#xa0;years) were recruited and divided in four groups according to presence/absence of CKD, defined as reduced estimated glomerular filtration rate (eGFR&#x2009;<&#x2009;60&#xa0;ml/min/m2) calculated using the creatinine-based Berlin Initiative Study-1 (BIS1) equation, and to presence/absence of hypertension (systolic blood pressure&#x2009;&#x2265;&#x2009;140 and/or diastolic blood pressure&#x2009;&#x2265;&#x2009;90&#xa0;mmHg). Subjects were analysed for selected SNPs spanning the SLC7A8 and SLC3A2 loci by Sequenom MassARRAY iPLEX platform. RESULTS: The most significant SNP at the SLC3A2 (4F2hc) locus was rs2282477-T/C, with carriers of the C-allele having a lower chance to develop hypertension among CKD affected individuals [OR&#x2009;=&#x2009;0.33 (CI 0.14-0.82); p&#x2009;=&#x2009;0.016]. A similar association with hypertensive CKD was found for the SLC7A8 (LAT2) rs3783436-T/C, whose C-allele resulted associated with decreased risk of hypertension among subjects affected by CKD [OR&#x2009;=&#x2009;0.56 (95% CI 0.35-0.90; p&#x2009;=&#x2009;0.017]. The two variants were predicted to be potentially functional. CONCLUSIONS: The association between SLC3A2 and SLC7A8 variants to hypertension development in patients with renal failure could be linked to changes in L-DOPA uptake and consequently dopamine synthesis. Although the associations do not survive correction for Bonferroni multiple testing, and additional research is needed, our study opens new avenues for future basic and translational research in the field of hypertensive CKD.

Aged↗
PubMed2004

Pentoxifylline: a potential therapy for chronic kidney disease.

Almost all forms of chronic kidney disease progressing to end-stage kidney failure are characterized by diffuse fibrosis, a final common pathway converging from multiple pathogenetic networks regardless of the initial injury. Four principal interventions including glycaemic and blood pressure control, dietary protein restriction, and angiotensin II blockade have been proven to slow progression of diabetic and/or non-diabetic chronic kidney disease. However, the ultimate solution to halt disease progression in the long term is still pending. Because of the pathogenetic complexity of kidney disease, multidrug intervention with the least side-effects should, without doubt, be the next step to stop kidney disease progression. Animal and cellular studies have demonstrated the rationale for pentoxifylline (i.e. its effects against cell proliferation, inflammation, and extracellular matrix accumulation) in the treatment of chronic kidney disease induced by immune- or non-immune-mediated mechanisms. Limited human studies have proven its efficacy in reducing proteinuria in patients with diabetes receiving angiotensin-converting enzyme inhibitors, and in patients with nephrotic syndrome refractory to conventional immunosuppressive therapy. Moreover, monotherapy with pentoxifylline markedly reduces proteinuria in patients with membranous nephropathy. Further studies are required to examine whether pentoxifylline can improve the renal outcome in patients receiving interventions with proven efficacy.

Animals↗
PubMed1990

The role of ischemia in acquired cystic kidney disease.

Acquired cystic kidney disease (ACKD) is the result of cyst formation in failing noncystic kidneys. This condition occurs in patients with chronic renal failure and becomes more common with increasing time on renal replacement therapy. Its complications include hemorrhage and tumor formation, which have acquired greater significance as more patients are started on dialysis treatment. The causes of ACKD remain speculative thus far. Its occurrence in nondialyzed patients suggests that dialysis itself is not a necessary factor in its pathogenesis. Five cases of severe unilateral renovascular disease and associated cyst formation are reported. The authors conclude that ACKD may derive from primary renovascular occlusion or from the secondary arterial and arteriolar occlusions seen in the end-stage kidney.

Aged↗
PubMed2004

Ability of troponin T to predict angiographic coronary artery disease in patients with chronic kidney disease.

Association between angiographic coronary artery disease and cardiac troponin T levels has been observed in patients with normal kidney function; however, this association remains unsettled in patients with chronic kidney disease (CKD) or end-stage renal disease (ESRD). Over a 12-month period we retrospectively reviewed coronary angiograms (CAs) performed in 194 hospitalized patients with presumed acute myocardial injury. About 50% of the ESRD and 30% of the CKD patients had normal CAs. Troponin T levels significantly correlated with CAs in patients with normal kidney function (r = 0.4, p = 0.005) but not in ESRD and CKD patients (r = 0.2, p = NS, respectively).

Coronary Angiography↗
PubMed1999

Evaluation of colonic diverticular disease in autosomal dominant polycystic kidney disease without end-stage renal disease.

A previous study had shown an increased prevalence (83%) of diverticula among patients with autosomal dominant polycystic kidney disease (ADPKD) with end-stage renal disease (ESRD) compared with other ESRD patients without ADPKD (32%). Others have also suggested an increased risk for diverticular complications in renal transplant recipients with ADPKD. To determine whether there was an increased occurrence of diverticula among non-ESRD patients with ADPKD, we studied 55 patients with ADPKD who were not receiving renal replacement therapy compared with 12 unaffected family members (non-ADPKD) and 59 random patients who had undergone barium enemas (control [C]). No study patient had a history of diverticular disease. All patients underwent a double-contrast barium enema after administration of glucagon. The occurrence, number, location, and size of diverticula were noted. There was no significant difference among the three groups in regard to sex (men: ADPKD, 42% versus non-ADPKD, 42% versus C, 37%) or age (ADPKD, 49.3 +/- 0.7 versus non-ADPKD, 51.2 +/- 2.1 versus C, 49 +/- 1 years). There was no significant difference in the percentage of patients with diverticula (ADPKD, 47% versus non-ADPKD, 58% versus C, 59%), the percentage with only right-colon diverticula (ADPKD, 5% versus non-ADPKD, 17% versus C, 5%), the mean number of diverticula in patients with diverticulosis (ADPKD, 13.8 versus non-ADPKD, 7.9 versus C, 9.9 diverticula), or the size of the largest diverticula (ADPKD, 9.5 versus non-ADPKD, 10.4 versus C, 10.5 mm). There was no significant difference in these variables between the patients with ADPKD with a creatinine clearance greater than 70 mL/min/1.73 m(2) (n = 25) or less than 70 mL/min/1.73 m(2). This study does not show the greater prevalence of diverticular disease in non-ESRD patients with ADPKD compared with the general population. Thus, patients with ADPKD need not be considered at greater risk for diverticular disease than the general population.

Diverticulum, Colon↗
PubMed1998

Seminal megavesicles with adult polycystic kidney disease.

Adult polycystic kidney disease has been found in association with pathological dilatation of the seminal vesicles in six patients. These men appeared normal on clinical examination, but had azoospermia or severe oligozoospermia. They were investigated by scrotal exploration with vasography, renal and transrectal ultrasound scans (TRUS), and percutaneous puncture of the seminal vesicles in one case, before and after resection of the ejaculatory ducts. This revealed that the gross dilatation of the seminal vesicles was not caused by obstruction, but appeared to be due to atonicity (megavesicles). These ultrasonic appearances, when described previously, were incorrectly thought to be due to seminal vesicle cysts.

Adult↗