Gitelman syndrome with normocalciuria - a case report.

BACKGROUND: Gitelman Syndrome (GS) is a hereditary tubulopathy associated with a biallelic inactivating mutations of the SLC12A3 gene encoding the thiazide-sensitive sodium-chloride cotransporter (NCCT). The typical clinical manifestation is a hypokalemic metabolic alkalosis with significant hypomagnesemia, and low urinary calcium excretion. Hypocalciuria is widely believed to be a hallmark of GS that distinguishes it from Barter's syndrome, presenting as hypercalciuria. The pathomechanism of hypocalciuria in GS is not fully elucidated. Up to date, a clinical course of GS with normocalciuria has been reported only in men, while women have a milder course of the disease with typical hypocalciuria, which is believed as the result of sex hormone. Additionally, there is a growing evidence that calcium channels of the distal nephron could be regulated by a variety of hormones, including aldosterone (Aldo). CASE PRESENTATION: We present the case of a 28-year-old Caucasian woman with asymptomatic, chronic hypokalemia, hypomagnesemia, hypochloremic alkalosis and normal urinary calcium excretion. A high renin levels with normal concentration of Aldo in serum have also been found. The values of blood pressure were low. Based on genetic studies, two heterozygous mutations in the trans position were confirmed: c.2186G>T (p.Gly729Val) and c.1247G>C (p.Cys416Ser) in the SLC12A3 gene, which ultimately confirmed the diagnosis of GS. CONCLUSIONS: We report here the first case of genetically confirmed GS manifested as normocalciuria in a Caucasian woman. Thus, our result does not confirm a role of sex hormones on the level of calciuria. Based on the results of normal Aldo concentration despite high renin level in our patient, we hypothesized that Aldo may be connecting with the level of urinary calcium excretion in patients with the GS.

Fructose-Rich Diet Is a Risk Factor for Metabolic Syndrome, Proximal Tubule Injury and Urolithiasis in Rats.

Excessive consumption of fructose (FR) leads to obesity, metabolic syndrome (MS) and insulin resistance, which are known risk factors for kidney stones. The epidemiological study has suggested the association between fructose consumption and urolithiasis, but the precise mechanism is still not well understood. Male Wistar rats were assigned for 8 weeks to three groups with different FR content in diet: RD (n = 5)-regular diet with a FR < 3%; F10 (n = 6)-regular diet with an addition of 10% Fr in drinking water; F60 (n = 5)-60% FR as a solid food. Serum concentration of FR, creatinine (Cr), insulin (Ins), triglycerides (Tg), homocysteine (HCS), uric acid (UA), calcium (Ca), phosphate (Pi), magnesium (Mg) and sodium (Na) were measured. Based on 24 h urine collection the following tests were performed: urine pH, proteinuria (PCR), excretion of N-Acetyl-(D)-Glucosaminidase (NAG), monocyte chemoattractant protein (MCP-1), uric acid (uUAEx), phosphate (uPiEx), calcium (uCaEx), magnesium (uMgEx) and sodium (uNaEx). The creatinine clearance (CrCl) was calculated. Calcium deposits in kidney sections were examined using hematoxylin and eosin (HE) and von Kossa stains. The rats on F10 and F60, as compared to the RD diet, showed a tendency for lower CrCl, higher HCS level and some features of MS as higher Ins and TG levels. Interestingly, F10 (fluid) versus F60 (solid) diet led to higher serum Ins levels. F10 and F60 versus RD demonstrated higher urinary excretion of MCP-1 and NAG which were suggestive for inflammatory injury of the proximal tubule. F10 and F60 as compared to RD showed significantly lower uUAEx, although there were no differences in clearance and fractional excretion of UA. F60 versus RD induced severe phosphaturia (>30×) and natriuria (4×) and mild calciuria. F10 versus RD induced calciuria (3×), phosphaturia (2×) and mild natriuria. Calcium phosphate stones within the tubules and interstitium were found only in rats on FR diet, respectively, in two rats from the F10 group and another two in the F60 group. The rats which developed stones were characterized by significantly higher serum insulin concentration and urinary excretion of calcium and magnesium. A fructose-rich diet may promote development of calcium stones due to proximal tubule injury and metabolic syndrome.

Coronary artery calcification and large artery stiffness in renal transplant recipients.

PURPOSE: Coronary artery calcification (CAC) is an independent predictor of cardiovascular (CV) events in renal transplant recipients (RTR). Carotid-femoral pulse wave velocity (PWV), a non-invasive measure of large artery stiffness, also predicts CV events in RTR. The study investigated the relationship between CAC and PWV in RTR and assessed the performance of PWV measurement in predicting CAC. PATIENTS/METHODS: The study was performed as cross-sectional analysis in 104 RTR. CAC was determined as total calcium score (CS) and calcium mass (CM). Carotid-femoral PWV was also measured. Sensitivity, specificity and receiver operating characteristic (ROC) curve were used to assess the performance of PWV as diagnostic test for presence of CAC. RESULTS: CAC was found in 69% of participants. PWV was higher in RTR with CAC than in RTR without CAC (10.2±2.2 vs. 8.6±15; p<0.001). In univariate analysis CS was significantly correlated with age, duration of hypertension, waist circumference, PWV, hemoglobin concentration, and serum glucose. In multiple linear regression analysis CS was independently associated with age only, but not with PWV. Sensitivity and specificity of PWV>7.6m/s as cut-off for detecting CAC>0 was 0.889 and 0.406, respectively. Sensitivity and specificity of PWV>10.2m/s as cut-off for detecting severe CAC (CS>400) was 0.319 and 0.969, respectively. CONCLUSIONS: The study confirmed high prevalence of coronary artery calcification in renal transplant recipients. The study does not support the hypothesis that aortic stiffness is independently associated with coronary artery calcification in RTR. PWV measurement may be useful in excluding severe CAC in RTR.

Abdominal collateral vein as an unconventional vascular access for hemodialysis in patient with central vein occlusion.

A 65-year-old female patient with chronic kidney disease stage 5 and a history of spleen neoplasm with dissemination within peritoneum is presented. During 5 years of hemodialysis therapy, bilateral occlusion of brachiocephalic and iliac vein developed as a consequence of vein catheterization. An attempt to cannulate inferior vena cava was unsuccessful. A cannulation of dilated collateral abdominal veins with dialysis needles allowed to perform several hemodialysis sessions in the patient.

Impact of fructose diet and renal failure on the function of pancreatic islets.

OBJECTIVES: This study was designed to evaluate the impact of fructose-rich diet and chronic kidney disease (CKD) on the in vitro function of pancreatic islets. METHODS: Fifty-four rats were divided into 3 equal groups as follows: control, rats with CKD 1/2 that underwent surgical uninephrectomy, and rats with CKD 5/6 that underwent uninephrectomy and kidney cortex mass resection. Each group was further assigned to 3 diet protocols--regular diet, regular diet with 10% fructose (F10), and 60% fructose-rich diet (F60). After 8 weeks of insulin administration, C-peptide, glycated hemoglobin level, serum urea nitrogen, creatinine clearance, and homeostasis model assessment of insulin resistance were evaluated. Static glucose insulin stimulation test of isolated pancreatic islets and histologic analysis of pancreatic tissue were performed. RESULTS: The F10 diet increased the levels of insulin and C-peptide in all groups. Homeostasis model assessment of insulin resistance was increased in all animals fed with fructose. The elevated levels of creatinine and diminished creatinine clearance were detected in CKD 5/6 rats fed with 60% fructose-rich diet. The F10 diet resulted in high levels of serum insulin and C-peptide and glucose-stimulated insulin secretion. Fructose-rich diet increased the islet size and number, with irregular morphology and exocrine tissue fibrosis. CONCLUSIONS: The fructose-rich diet accelerates the progression of CKD and affects the pancreatic islet function.

Advanced glycation end products and arterial stiffness in patients with diabetic nephropathy and patients with chronic kidney disease without diabetes.

INTRODUCTION:  Formation of advanced glycation end­products (AGEs) is increased in diabetic patients. Impaired renal function also elevates AGE accumulation. Pulse wave velocity (PWV) is a measure of arterial stiffness and a prognostic parameter. An association between AGEs and arterial stiffness was observed in hemodialyzed patients. OBJECTIVES:  We investigated the relationship between plasma AGE concentration and arterial stiffness in nondialyzed patients with diabetic nephropathy and those with chronic kidney disease (CKD) without diabetes. PATIENTS AND METHODS:  PWV measurement was performed in 24 patients with CKD and diabetic nephropathy (DN), 36 patients with CKD and without diabetes, and 19 controls. To assess AGE concentrations, plasma fluorescence spectra were recorded.  RESULTS:  Patients with and without diabetes did not differ with respect to the glomerular filtration rate (33 ±13 vs. 32 ±14 ml/min/1.73 m2, respectively). The AGE concentration was significantly higher in patients with DN compared with those without diabetes and controls (21.1 ±6.8 vs. 12.3 ±3.1 vs. 7.8 ±1.2 AU/ml, respectively; P <0.001). PWV was also significantly higher in patients with DN compared with those without diabetes and controls (13.7 ±4.3 vs. 10.1 ±2.4 vs. 8.4 ±1.6 m/s, respectively; P <0.05). A significant correlation was found between AGEs and PWV (r = 0.39, P <0.01) in patients with CKD. In a multiple regression analysis, PWV was independently associated with age, DN, and systolic blood pressure, but not with AGEs (R2 = 0.45).  CONCLUSIONS:  Accumulation of AGEs and arterial stiffness are increased in patients with CKD, particularly in those with DN; however, the results are not sufficient to confirm the causal role of AGE accumulation in arterial stiffening in CKD. AGEs should be considered as a potential therapeutic target in patients with CKD.

Decreased hypoxia-inducible factor-1α in gastrocnemius muscle in rats with chronic kidney disease.

BACKGROUND/AIMS: Hypoxia-inducible factor (HIF)-1α is responsible for increased expression of genes engaged in angiogenesis. Our previous study indicated capillary rarefaction and atrophy of glycolytic fibers, mainly in locomotor muscles of uremic animals. Perhaps these changes are secondary to disturbances of HIF-1α in skeletal muscles. METHODS: Expression of HIF-1α at mRNA and protein levels, as well as mRNA of vascular endothelial growth factor A (VEGF-A), vascular endothelial growth factor receptor (VEGFR)-1, VEGFR-2, endothelial nitric oxide synthase (eNOS) and inducible nitric oxide synthase (iNOS), in gastrocnemius muscle (MG) and longissimus thoracic muscle (ML) were measured by RT-PCR and Western blot. Rats were randomized to subtotal nephrectomy (CKD5/6), uninephrectomy (CKD1/2) or sham operation (controls). RESULTS: For CKD5/6 versus controls, mRNA levels for HIF-1α, VEGF-A, VEGFR-1 and VEGFR-2 were significantly reduced only in MG, while eNOS was significantly decreased and iNOS was significantly increased only in ML. Western blot analysis indicated significantly increased HIF-1α protein levels in MG and ML from CKD1/2 animals versus controls, whereas in the CKD5/6 group, the level of HIF-1α protein decreased significantly in MG and increased significantly in ML versus controls and CKD1/2. CONCLUSION: The reduced expression of HIF-1α mRNA and protein in locomotor muscle from CKD5/6 animals may be involved in the pathogenesis of uremic myopathy. Increased expression of iNOS in the postural muscles may act as a protective factor through HIF-1α stabilization.

Low-fructose diet lowers blood pressure and inflammation in patients with chronic kidney disease.

BACKGROUND: Fructose has been strongly linked with hypertension, hyperuricemia and inflammation in experimental models and humans. However, the effect of low-fructose diet on inflammation, hyperuricemia and the progression of renal disease has not yet been evaluated in patients with chronic kidney disease (CKD). METHODS: Twenty-eight patients (age 59 ± 15 years, 17 males/11 females) with Stages 2 and 3 CKD were switched from a regular (basal) (60.0 g/24 h) to a low (12.0 g/24 h) fructose diet for 6 weeks, followed by a resumption of their regular diet for another 6 weeks. Diet was monitored by a dietician. At the baseline, low- and regular-fructose diet ambulatory blood pressure (BP) was measured and blood sampled for renal function (creatinine), inflammatory markers, fasting glucose and insulin and serum uric acid. Twenty-four-hour urine collections were also obtained for creatinine, uric acid, monocyte chemotatic protein-1, transforming growth factor-beta and N-acetyl-beta-D-glucosaminidase. RESULTS: The low-fructose diet tended to improve BP for the whole group (n = 28), while significant reduction of BP was only seen in dippers (n = 20) but not in non-dippers (n = 8). No effects on estimated glomerular filtration rate (eGFR) or proteinuria were observed. Serum uric acid was lowered non-significantly with low-fructose diet (7.1 ± 1.3 versus 6.6 ± 1.0 mg/dL, P < 0.1), whereas a significant decrease in fasting serum insulin was observed (11.2 ± 6.1 versus 8.2 ± 2.9 mIU/mL, P < 0.05) and the reduction persisted after return to the regular diet. A slight but not significant reduction in urinary uric acid and fractional uric acid excretion was observed while the patients were on the low fructose diet. The low-fructose diet also decreased high sensitivity C-reactive protein (hsCRP) (4.3 ± 4.9 versus 3.3 ± 4.5 mg/L; P < 0.01) and soluble intercellular adhesion molecule (sICAM) (250.9 ± 59.4 versus 227 ± 50.5 ng/mL; P < 0.05). The hsCRP returned to baseline with resumption of the regular diet, whereas the reduction in sICAM persisted. CONCLUSION: Low-fructose diet in subjects with CKD can reduce inflammation with some potential benefits on BP. This pilot study needs to be confirmed by a larger clinical trial to determine the long-term benefit of a low-fructose diet compared to other diets in subjects with CKD.

Lack of effect of the CD14 promoter gene C-159T polymorphism on nutritional status parameters in hemodialysis patients.

BACKGROUND: CD14 is a membrane glycoprotein that acts as a co-receptor for the detection of bacterial lipopolysaccharide (LPS). Mutual interaction between CD14 and LPS plays an important role in the innate immune system. Increased serum soluble CD14 levels have been described in hemodialysis (HD) patients, and linked to increased mortality risk, inflammation and protein-energy wasting. The expression of CD14 may be influenced by CD14 promoter gene C-159T polymorphism. This study aimed to clarify the possible association between CD14 promoter gene C-159T polymorphism and nutritional status in hemodialysis patients. MATERIAL/METHODS: The study population consisted of 185 (104 males; 81 females) long-term HD patients treated in 5 dialysis centers. The control group consisted of 112 apparently healthy volunteers (32 males and 80 females). Nutritional status was assessed using a modified SGA scale, and anthropometric methods (BMI, WHR, waist, hip and mid-arm circumferences, biceps, triceps, subocular and subscapular skinfolds). Biochemical parameters evaluated included: CRP, albumin, creatinine, urea, cholesterol, triglycerides and TIBC. CD14 promoter gene C-159T polymorphism was determined by restriction fragment length polymorphism, after digestion of the PCR product with Hae III restriction endonuclease. RESULTS: Genotype and allele frequencies were similar to controls and compliant with Hardy-Weinberg equilibrium. No between-group differences were detected in measured variables with the exception of lower triglyceride levels in carriers of C allele in comparison to TT genotype. CONCLUSIONS: CD14 promoter gene C-159T polymorphism does not seem to be associated with nutritional status parameters in HD patients. It does seem, however, to influence triglyceride blood levels.

[Patient with chronic kidney disease and primary or tertiary hyperparathyroidism--case report]. / Pierwotna czy trzeciorzedowa nadczynnosc przytarczyc u chorej na przewlekla chorobe nerek--opis przypadku.

Primary hyperparathyroidism (PHPT) is a clinical state of excessive parathyroid hormone (PTH) secretion. The clinical profile of PHPT depends on duration of disease, PTH concentration, hypercalcemia and coexisting disorders. The symptoms associated with PHPT are neither typical nor specific. Asymptomatic PHPT is often diagnosed accidentally, based on laboratory results. The article presents case of 31-year old woman with chronic kidney disease (CKD) stage 4, persistent hypercalcemia, hypophosfataemia. Tertiary hyperparathyroidism (THPT) is most often situation when these disturbances occur but in this clinical situation CKD and PHPT is more likely. Paraendocrynopathy is also taken into consideration. Diagnostic methods estimate serum concentration of calcium and phosphate on each stage of CKD allowed to exclude THPT. Cinacalcet treatment followed by parathyroid surgery reduced serum calcium concentration.

Acquired hemophilia: a case report.

Acquired hemophilia is a severe bleeding diathesis that affects both males and females. It is caused by suddenly appearing autoantibodies that interfere with coagulation factor VIII activity. This disorder is characterized by spontaneous and post-traumatic subcutaneous bleeds and massive mucosal hemorrhages. We report in the current article a case of acute renal failure and bleeding from the urinary tract caused by idiopathic acquired hemophilia in a 54-year-old woman. Hemostatic tests indicated prolonged activated partial thromboplastin time (APTT) to 107.8 sec (norm 26-36 sec), normal value of the prothrombin index which was 82% (norm 70-130%), increased fibrinogen concentration to 583 mg/dl (normal value 200-400 mg/dl), the bleeding time was 5 min and 20 s (norm < 10 min) and the platelet count was 366 x 10(9)/l (norm 130-400 x10(9)/l). The autoantibody against factor VIII in a titer of 121 Bethesda Units/ml (BU/ml) and decreased factor VIII activity to 2% (norm 50-150%) with normal plasma concentration of factor IX. Activated (FEIBA, Baxter) and nonactivated prothrombin complex concentrates (factor IX concentrate) have been used in the treatment of bleeding episode. Immunosuppressive treatment with the combination of oral prednisone 60 mg/24h and cyclophosphamide 150 mg/24h was administered in order to remove the factor VIII inhibitor. Reduction of the factor VIII inhibitor titer to 38 BU/ml and increase of factor VIII activity to 4% was initially achieved. This treatment has been continued for two years and led to normalization of hemostatic parameters (APTT 26 sec, factor VIII activity 108%) which means a total removal of factor VIII inhibitor.

Influence of different stages of experimental chronic kidney disease on rats locomotor and postural skeletal muscles microcirculation.

BACKGROUND: Chronic kidney disease (CKD) is associated with muscle excess fatigue and diminished maximal whole body oxygen consumption, which in part could be depended on poor muscle microcirculatory network. The aim of this study was to assume the influence of different stages of CKD on microcirculation vessels in functionally different skeletal muscles--locomotor, the gastrocnemius muscle, and postural, the longissimus thoracis muscle. METHODS: Male Wistar rats underwent sham operation (CON), uninephrectomy (CKD 1/2) and subtotal nephrectomy (CKD 5/6). Muscle samples were stained for an alkaline phosphatase to differentiate capillaries. The number of capillaries was estimated by a single observer in 10 microm transverse sections by point counting at a magnification of x 125 using an Image Analysis System Q 500 MC of Leica. Blood pressure and serum creatinine, haptoglobin, MCP-1, VEGF, and PDGF were measured. RESULTS: There were significant differences (p < 0.05) in CD (number of capillaries per 1 mm(2) of muscle tissue), C:F (capillary to fiber ratio), and CC/F (capillary contact per fiber). The CKD 1/2 group in gastrocnemius and longissimus muscle had 53% and 33% lower C:F; 56% and 33% lower CD; and 44% and 20% less CC/F than CON, respectively. The CKD 5/6 group in gastrocnemius and longissimus muscle had 46% and 20% lower C:F; 47% and 11% lower CD; and 48% and 25% less CC/F versus control, respectively. Blood pressure was higher in CKD 5/6 vs. CKD 1/2 and CON (145/95 vs. 107/87 and 119/77 mmHg, p < 0.05, respectively). CKD 5/6 had higher creatinine than CKD 1/2 and CON (1.22 vs. 0.83 and 0.74 mg/dL, p < 0.05, respectively). Haptoglobin was higher in CKD 1/2 and CKD 5/6 versus CON (1.68 and 1.63 vs. 0.70 mg/mL, p < 0.05, respectively). MCP-1 was higher in CKD 5/6 and CKD 1/2 versus CON (609 and 489 vs. 292 pg/mL, p < 0.05, respectively). There were no significant differences in serum growth factors concentration between groups. CONCLUSION: Capillary rarefaction is present in early stages of CKD. These changes are independent of blood pressure and progression of CKD. We suspected that muscle function has a big impact on microvasculature as capillaries rarefaction has been reduced more in locomotor than postural skeletal muscle.

Anderson-Fabry disease: diagnostic problems from gastrointestinal manifestations to the diagnosis of kidney disease.

We report a case of a 52-year-old male who has been diagnosed for many years because of chronic diarrhea and proteinuria with concomitant gradually progressing chronic kidney disease. Diagnostic problems associated with the initial diagnosis of amyloidosis as a primary cause of the patient's complaints have been described. Anderson-Fabry disease (AFD) was suspected following comprehensive evaluation that resulted eventually in the exclusion of amyloidosis and the echocardiographic examination showing hypertrophic cardiomyopathy in the patient with no history of hypertension and aortic valve defects. The diagnosis of AFD was confirmed by results of enzymatic tests.

Cardiac troponin I in patients with chronic kidney disease treated conservatively or undergoing long-term haemodialysis.

BACKGROUND: Cardiac troponin I (cTnI) has been shown to be a specific marker of myocardial damage in the general population. In patients suffering from chronic kidney disease (CKD) cTnI may be increased in serum without other signs of acute myocardial damage confusing the diagnosis. AIM: To compare cTnI concentration in CKD patients, treated conservatively or with haemodialysis, with healthy controls, and to evaluate the cardiovascular risk factor profile in these groups. METHODS: The study population consisted of three groups: group I (n=10, 5 women, 5 men, mean age 32+/-4 years) - healthy, young volunteers without kidney diseases with creatinine clearance (CrCl) 97.13+/-23.24 ml/min; group II (n=21, 8 women, 13 men, mean age 51+/-15 years) - patients with CKD in stages 3-5 with CrCl=34.04+/-18.34 ml/min; and group III (n=30, 14 women, 16 men, mean age 50+/-14 years) - patients on long-term haemodialysis. The cTnI level was measured using an AxSYM analyzer (Abbott). In group III blood was taken before the haemodialysis session. The high sensitivity C-reactive protein (hsCRP), haemoglobin, parathyroid hormone (PTH) and phosphorus levels were determined. Blood pressure was also recorded. Echocardiography was performed and left ventricular mass index (LVMI) was calculated on the basis of the Devereux and Reichek formula. RESULTS: Compared with controls, the cTnI values were significantly higher in patients from group III and tended to be higher in patients from group II (0.01+/-0.03 vs. 0.063+/-0.08 and 0.066+/-0.162 ng/ml, respectively, p <0.05 and NS). In 46% of haemodialysed patients cTnI concentration was above the value of the 99th percentile in the apparently, healthy population but did not exceed the acute myocardial infarction diagnostic cut-off. The high sensitivity C-reactive protein value was significantly higher in groups III and II versus controls (4.92+/-5.12 and 2.26+/-2 vs. 0.85+/-0.48 mg/dl, p <0.05 respectively). The LVMI values were significantly higher in groups III and II than in controls (159+/-46 and 113+/-35 vs. 81+/-14 g/m2, respectively). There was a significant correlation between hsCRP and LVMI in group II (r=0.49, p <0.05). Blood pressure was significantly higher in groups III and II compared to controls (129+/-25 and 137+/-19 vs. 116+/-7 mmHg, respectively). Patients from group III had significantly decreased haemoglobin value and increased PTH as well as phosphorus concentration compared to subject from group II and controls. CONCLUSION: Chronic kidney disease is associated with accumulation of cardiovascular risk factors and increased cTnI concentration.

Inflammation, malnutrition and vascular contraction in experimental chronic kidney disease.

BACKGROUND: Inflammation is a well-defined factor influencing the development of cardiovascular complications in chronic renal failure. The aim of this study was to examine systemic inflammatory state defined by the level of serum haptoglobin, local inflammation defined by monocyte chemoattractant protein-1 (MCP-1) level and arterial response to phenylephrine in different stages of renal failure. METHODS: Experiments were performed on male Wistar rats, weighing 290-380 g. The rats were divided into 4 groups: I (control) was shame-operated (n=12); II underwent 1/2 nephrectomy (n=12); III, 3/4 nephrectomy (n=8); IV 5/6 nephrectomy (n=12). After 4 weeks, blood pressure (BP) in carotid artery was measured, and blood was collected for blood urea nitrogen, creatinine, albumin, haptoglobin and MCP-1. We compared the smooth muscle contractility after stimulation of alpha1-adrenoreceptor with phenylephrine in all groups. The constriction of artery was measured as the increase in perfusion pressure at a constant flow of the perfusion fluid. Cumulative response curves (CRCs) were obtained using the van Rossum method. RESULTS: We observed a significant shift of CRCs to the left in group III (calculated half-maximal contraction [EC50] was 1.55 x 10(-7) M/L vs. 7.71 x 10(-7) M/L in control) and a nonsignificant shift of CRCs to the left in group II (3.62 x 10(-7) M/L). Unexpectedly, rat tail arteries from the rats in the 5/6 nephrectomy group were characterized by diminished contraction response to phenylephrine (EC50 9.57 x 10-7 M/L). Systemic inflammation defined by haptoglobin level occurred in the 1/2 nephrectomy group and did not increase in more advanced stages of renal disease. Local inflammation (MCP-1 level) increased together with the renal failure progression. We found a positive correlation between MCP-1 level and haptoglobin only in the 5/6 nephrectomy group (r=0.65; p<0.01). CONCLUSION: The inflammatory state which affects vascular smooth muscle cells plays a key role in determining vascular contraction and resistant artery tone.

[Diagnostic and prognostic value of cardiac troponins in patients with chronic kidney disease]. / Znaczenie diagnostyczne i prognostyczne troponin w przewleklej chorobie nerek.

In the contemporary diagnostics of myocardial infarction importance of the role of biochemical markers such as troponins, CK, CK-MB, CK-MB mass has been underscored. In the paper biochemical aspects of their composition and the kinetics of troponin realase by the heart have been presented. Frequent occurrence of cardiovascular diseases in population of patients with chronic kidney disease, being the results of coexistence of traditional and non-traditional risk factors, has been highlighted. Also, difficulties in diagnostics of acute coronary symptoms in this group of patients have been pointed to. In the article the factors leading to non- specific elevation of serum troponin levels in this patient population, as well as the influence of the degree of kidney function impairment and influence of the type of dialysis on troponin levels have been discussed. Based on the analysis of the major clinical trials the role of troponin in diagnostics of myocardial infarction and long-term prognosis in patients with chronic kidney disease have been discussed. Other clinical conditions in which serum troponin level elevation is observed have been although discussed.

[Predictors of successful renal artery revascularization in atherosclerotic renovascular disease]. / Czynniki prognostyczne powodzenia zabiegu rewaskularyzacji tetnicy nerkowej u chorych z przewlekla choroba niedokrwienna nerek.

Atherosclerotic renovascular disease (ARVD) is defined as a reduction in glomerular filtration rate in patient with significant renovascular bilateral occlusive disease or unilateral in a solitary kidney. ARVD is a frequent and potentially avoidable cause of end stage renal failure and the need for replacement therapy among person above 50 years old. Use of balloon angioplasty with stenting or surgical repair has been shown to improve renal potency, but there is no clear evidence that it prevents further progressive decline of renal function or blood pressure, compared to medical therapy alone. It is now recognized that severity of histopathologic damage is an important determinant and predictor of renal functional outcome. Proteinuria increases with declining renal failure and reflects the severity of parenchymal damage. Proteinuria and high renal resistance index are associated with glomerular damage and altered intrarenal perfusion. They aren't linked to renal artery stenosis (RAS) grade. Recent study indicate that abrupt decline in renal function reflects reversibility after revascularization. This should probably be undertaken in RAS patients with rapidly deteriorating renal function, refractory hypertension and in whom plasma creatinine concentration has increased by >20% during one month long administration of angiotensin-converting enzyme inhibitor. Renal biopsy may be useful to evaluate patient who will have advantage from revascularization.

Morphometry of the pancreas in human foetuses.

With the use of conventional anatomical dissection, radiography, digital and statistical analysis, morphometry and skeletopy of the pancreas was carried out in 60 human foetuses of both sexes (28 female, 32 male) between the 17th and 40th week of intrauterine life. The material was fixed in a 10% formalin solution. The age of the foetuses was determined by crown-rump (CR) length measurement on the basis of the Iffy et al. tables. Photographic documentation was made and then digitally processed in the Computer Image Digital Analysis System. The following parameters were taken into account: the length and width of 3 parts of the pancreas, namely the head, corpus and tail. Additionally, radiograms were made to obtain a projection of the gland on the vertebral column. Development of the pancreas was correlated with the age of the foetuses calculated on the basis of crown-rump (CR) length measurements. The correlation coefficient with CR was 0.998 for the pancreas length, 0.709 for the width of the head, 0.703 for the width of the corpus and 0.712 for the width of tail. Gender dimorphism was not found (p > 0.05) with regard to the morphometry of the pancreas. In the material under examination the pancreas did not change its position in relation to the vertebral column. The head projected on the vertebral column in the range Th(12)-L(2) (most frequently L(1)-L(2)), the corpus on Th(12)-L(2) and the tail on Th(11).

The pancreaticoduodenal arteries in human foetal development.

Knowledge of the course of the pancreaticoduodenal arteries is of great importance in pancreatic surgery. Lack of care in the preparation of these vessels may lead to ischaemia or necrosis of the duodenum, the first loop of the jejunum, the head of the pancreas and even the liver, bile ducts and transverse colon. In such events, the surgeon would need to diagnose the course of the vessels and their anastomoses intraoperatively. Anatomical dissection in this special area diminishes the risk of early complications in the form of bleeding and late complications in the form of narrowing of the anastomoses, fistulas, necrosis and intestinal ileus after surgical resection or drainage. The aim of the present study was to determine the variability of the pancreaticoduodenal arteries in human foetuses. The material examined consisted of 60 human foetuses of both sexes (33 male, 27 female) from spontaneous abortion or stillbirth and ranging in age from the 16th to 38th week of prenatal life. White latex solution to of volume between 15 ml and 30 ml was injected into the thoracic aorta. The results of this were that a typical pancreatic supply from the coeliac trunk and superior mesenteric artery was observed in all cases. The coeliac trunk, splenic artery and gastroduodenal artery also appeared invariably. However, variability was observed in further generations of branches. The gastroduodenal artery with its branches, the anterior and posterior pancreaticoduodenal arteries, was constantly present. Irrespective of the sex of the foetus, in 10% of cases a large vessel was observed which ran horizontally on the anterior surface of the pancreas from head to tail and which originated in the anterior superior pancreaticoduodenal artery. We termed this vessel the "anterior pancreatic artery". In all cases there were anterior and posterior pancreaticoduodenal arcades, but in two cases (3.3%) a double anterior pancreaticoduodenal arcade was observed.