Are other factors besides albuminuria important for the progression of HCV chronic hepatitis towards CKD? A survey from a hepatology department in western Romania.

UNLABELLED: HCV is an important cause of renal disease. Taal and Brenner have identified risk factors for CKD and have suggested that these risk factors be incorporated into a renal risk score analogous to the Framingham cardiovascular score. Given the high HCV-renal disease comorbidity, we sought to assess risk factors for CKD in patients with HCV chronic hepatitis. METHODS: One hundred-seventeen patients with HCV chronic hepatitis (mean age: 50.68 +/- 9.14 years; 86 female and 31 male) hospitalized in the Department of Hepatology during 2009 were enrolled into the study. All patients were assessed for the risk factors for CKD proposed by Taal and Brenner: albuminuria, diabetes mellitus, hypertension, obesity, anemia, hypercholesterolemia, hypertriglyceridemia, nephrotoxins, primary renal disease, associated urological disorder, cardiovascular disease and family history of CKD. Renal function (GFR-CKD-Epi) was also evaluated. STATISTICAL ANALYSIS: Pearson's correlation coefficient and Odds Ratio (OR) was performed using SPSS17 and Epi 3.2.2. RESULTS: The prevalence of albuminuria was 21.36%, of hypertension was 20.51%, of obesity was 21.36%, and hypercholesterolemia was present in 41.02% of the cases. Renal function was as follows: 10.25% (12/117) of the patients had a GFR < 60 mL/min/1.73 sqm.; 64.95% (76/117) of the patients had a GFR between 60-89 mL/min/1.73 sqm.; and 24.78% (29/117) had a GFR > or = 90 mL/min/1.73 sqm. CONCLUSIONS: Our study shows that HCV chronic hepatitis is associated with renal function impairment in a high percentage of patients. Prominent risk factors for CKD are present in these patients, such as albuminuria, hypertension, obesity, and hypercholesterolemia, which need to be actively searched and addressed therapeutically.

The solitary kidney--a nephrological perspective.

The solitary kidney (SK) is of special interest for practitioners because of the reduced number of nephrons as compared to persons who have 2 kidneys. It undergoes adaptive phenomena of hypertrophy and hyperfiltration that allow long-term evolution, but pathological situations might occur in the remnant kidney. In some persons with a SK, the adaptive phenomena can be associated with proteinuria, arterial hypertension (AH) and diminished Glomerular Filtration Rate (GFR). In very rare situations, diminution of renal function in patients with a SK can progress to end-stage renal disease (ESRD) and, totally exceptionally, it requires renal replacement therapy. The SK can be congenital or acquired. At present patients with a SK address themselves more and more frequently to nephrology services which monitor the evolution of both the congenital and the surgically acquired SK. The congenital SK possesses a higher number of nephrons (75%, as compared to 2 functional kidneys in a healthy person) than the surgically acquired SK - 50% nephrons. This makes adaptive phenomena differ. Secondary lesions sometimes appear later in case of the congenital SK. In other situations, no significant differences between the evolution of the congenital or acquired SK are registered. The congenital solitary kidney is often associated with congenital abnormalities of the kidney and of the urinary tract (CAKUT). This association increases the risk for chronic kidney disease and for evolution towards chronic renal failure. The congenital SK is also often associated with gynaecological and other abnormalities. The acquired solitary kidney can be due to nephrectomy on a pathological kidney which could not be conservatively treated or due to donation of a kidney for renal transplantation. The SK itself sometimes requires partial nephrectomy intervention, for example sparing surgery. Although the evolution is in most cases favorable, it requires attentive monitoring.

Biomarkers in assessing tubular lesions of the solitary kidney. The solitary kidney in special conditions.

The paper highlights the importance of tubular lesions of the solitary kidney (SK), identified and monitored by means of urinary biomarkers, mainly N-acetyl-beta-D-glucosaminidase (NAG), albumin, alpha 1-, and beta 2-microglobulin. It is considered that the assessment of a SK should be performed with four and not three parameters as it was usually done until recently: renal function, proteinuria and blood pressure (BP), to which biomarkers should be added. The solitary kidney can result after nephrectomy for kidney transplantation. In some countries living kidney donors represent the only option for performing kidney transplantation. The SK in living donors has generally a good evolution, although sometimes renal injury manifested by proteinuria, arterial hypertension (AH), or diminution of renal function does occur. Therefore, living donors require attentive monitoring. The SK is considered to have a good evolution (even in donors), in spite of alterations of the above-mentioned clinical and biological parameters. The very infrequent cases who evolve progressively towards renal failure are not predictable, which requires monitoring of all persons with a SK. The SK represents a special situation in case of association with a disease affecting the kidney, such as urinary tract infection (UTI), diabetes mellitus, or systemic lupus erythematosus (SLE). Pregnancy occurring in a person with a SK also needs attentive follow-up. Pregnancy associated diseases, such as preeclampsia occurring in patients with a SK, impose appropriate therapeutic behaviour. The SK remains a particular entity in nephrology which needs to be carefully monitored.

Pregnancy-induced hypertension--a particular pathogenic model. Similarities with other forms of arterial hypertension.

Hypertension is in 85 to 90% of cases of unknown etiology, in spite of efforts undertaken by modern medicine to elucidate it. Numerous experimental studies were conducted in order to explain the pathogeny of this disease. Recent observations revealed that during therapy with anti-VEGF medication,used in treating different forms of cancer, hypertension and proteinuria occur, and at kidney level endothelial injuries appear similar to pregnancy-related hypertension. Antiangiogenic factors, such as sFlt-1, are produced during pregnancy-induced hypertension, especially in preeclampsia. They block the circulating VEGF. Consequently, proteinuria, and sometimes oedema occur together with hypertension. Renal injuries are of glomerular endotheliosis type. It is appreciated that one can draw a parallel between these pathologic situations, as is ablative treatment of antiangiogenic medication (anti-VEGF) and pregnancy-induced hypertension, preeclampsia, respectively. Since in pregnancy-induced hypertension angiogenic factors have an important role, we analyse their implication in other types of hypertension, in myocardial infarction, and in endothelial dysfunction in the course of CKD. The main pathogenic mechanism of pregnancy-induced hypertension that causes the disease is placental ischaemia. This is followed by the placental release of pressor substances that are involved both in generalised endotheliosis that characterizes the disease, and in hypertension. The prototype hypertension caused by renal ischaemia is renal artery stenosis. Both pregnancy-induced hypertension and hypertension in renal artery stenosis have a similar factor in their pathogeny, that is organ ischaemia with production of consecutive pressor substances. Since this ischaemic factor can intervene in other forms of hypertension, its characterisation becomes of importance at present. Thus, pregnancy-induced hypertension in pregnancy can represent a real pathogenic model of hypertension that is reflected in non-pregnancy hypertension. The paper presents the particularities of pregnancy-induced hypertension, as well as its parallelism with other types of hypertension that are determined by organ ischaemia or that produce ablation of angiogenic factors.

Chronic kidney disease and the involvement of estrogen hormones in its pathogenesis and progression.

The kidney is under the influence of sexual hormones. Estrogens have a favourable role in the progression of some chronic renal diseases. Estrogen hormones act upon the nephron component cells, regulating several processes going on at this level. One of the most important actions of the estrogens is represented by the protective effect on the kidneys, estrogens attenuating glomerulosclerosis and tubulo-interstitial fibrosis. Thus, estrogens have nephroprotective effects. Phosphorus-calcium metabolism disturbances during chronic kidney disease are influenced by numerous regulatory factors: parathormone, vitamin D fibroblast growth factor, 23. Estrogens play an important part in disturbances of the phosphorus-calcium metabolism, co-operating with these factors. They exert favourable effects on renal osteodystrophy, the main consequence of phosphorus-calcium disturbances. Hormonal dysfunction in chronic kidney disease is clinically accompanied by sexual dysfunction that influences the life quality of these patients. In advanced stages of chronic kidney disease, especially in dialysed patients, these sexual dysfunctions can be more evident. Hormonal replacement therapy and estrogen therapy- receptor modulating therapy have an important role in correcting hormonal dysfunctions manifest in chronic kidney disease. Caution is necessary in case of a would-be pregnancy in patients with chronic kidney disease, given its risks and the complexity of the problem. Renal transplantation corrects to a great extent hormonal dysfunctions in chronic kidney disease.