Noninvasive evaluation of muscle mass by ultrasonography of quadriceps femoris muscle in End-Stage Renal Disease patients on hemodialysis.

BACKGROUND & AIMS: Protein-Energy Wasting (PEW) is a pathological condition of renal patients with advanced Chronic Kidney Disease characterized by a progressive reduction of energy and protein assets. Nutritional status assessment, especially for what concerns muscle mass, is essential for both the identification of patients at risk for the development of PEW, as well as monitoring the effects of nutritional interventions. Ultrasound methods are easily applicable at the bedside for quantitative assessment of skeletal muscle. The present study was aimed at evaluating quadriceps rectus femoris thickness (QRFT) and quadriceps vastus intermedius thickness (QVIT) in patients on chronic hemodialysis. METHODS: This was a prospective observational study. Three groups of adult patients were studied: young healthy subjects, well-nourished hospitalized patients with normal renal function, and End-Stage Renal Disease patients on hemodialysis (ESRD-HD). QRFT and QVIT were measured at two sites bilaterally (8 measures/patient) and were compared between groups, and also between subgroups of ESRD-HD patients stratified on the basis of conventional nutritional status parameters. RESULTS: We enrolled 35 healthy subjects, 30 hospitalized patients, and 121 ESRD-HD patients on hemodialysis. QRFT and QVIT of ESRD patients on hemodialysis were lower than those of both control groups (P < 0.001). After stratifying ESRD patients into subgroups based on nutritional variable cut-offs commonly used to define PEW in this clinical setting (BMI [≥ 23 vs <23 kg/m2], albumin [≥3.8 vs <3.8 g/dL]) and malnutrition inflammation score (MIS) status (<6 vs ≥6), QRFT and QVIT of patients with worse nutritional status were significantly lower than those of well-nourished ESRD-HD patients (P value range: <0.001 to <0.05). CONCLUSION: Skeletal muscle ultrasound is a simple and easily applicable bedside technique in the dialysis units, and could represent an adequate tool for the identification of patients with reduced muscle mass.

The renal effects of mineralocorticoid receptor antagonists.

Beyond its well known classic effects on renal water and electrolytes metabolism, an increasing amount of experimental and clinical evidence suggests that aldosterone contributes to the pathogenesis and progression of kidney disease. The binding of aldosterone on epithelial and non-epithelial cells of the kidney induces many deleterious effects, such as podocyte apoptosis and injury, mesangial cell proliferation and deformability and tubulointerstitial inflammation, finally resulting in glomerular fibrosis and sclerosis. Moreover, aldosterone acting by fast non-genomic mechanisms, may induce other potential deleterious effects on kidney function and structure. Indeed, many experimental studies have shown that aldosterone participates to the progression of kidney disease through hemodynamic and direct cellular actions and that antagonists of aldosterone may retard the progression of kidney disease, independently of effects on blood pressure. Therefore, blockade of the aldosterone pathway may prove to be a beneficial therapy for kidney disease. In this brief review we summarize the reported data that support an independent role of aldosterone in inducing kidney damage both in human and experimental models, and interventional studies that highlight how strategies aimed to antagonize its action may favorably modify the progressive decline of renal function in patient with kidney disease and in patients with extrarenal disease frequently associated with kidney function impairment.

Theoretical calculation of optimal depth in the percutaneous native kidney biopsy to drastically reduce bleeding complications and sample inadequacy for histopathological diagnosis.

BACKGROUND: In recent years percutaneous native kidney biopsy (PNKB) has become of very common use and safe enough for the patient if performed by skilled physicians; nevertheless, haemorrhagic complications or inadequate tissue sample for the diagnosis may occur. We report here the type and the adequacy rate of specimens for diagnosis and complication rate associated with PNKB performed in a single centre from May 2003 to December 2005 using a mathematical formula to determine the depth in centimetre where pushing the trigger. METHODS: In this prospective study we analysed data from 126 consecutive PNKB performed by the same two skilled nephrologists with the free hand technique using the 14-gauge automated biopsy gun under continuous sonographic control (Group I). The trigger was pushed exactly at the depth previously calculated by a mathematical formula: BW/H (body weight expressed in hectograms divided by patient height expressed in centimetres) less 0.5 (BW/H - 0.5). The type and the adequacy rate of specimens for diagnosis and the associated complication rate were retrospectively compared with data obtained from 123 consecutive PNKB performed from January 2001 to April 2003 by the same operators before using the mathematical formula described earlier (Group II). RESULTS: Of our series of 126 consecutive PNKD using the mathematical formula (Group I), only four subjects presented post-biopsy gross haematuria (3.2%) and three experienced symptomatic small subcapsular haematoma (2.4%). All biopsy specimens proved to be adequate for diagnosis (100%) with a mean of 22 glomeruli (range 5-60) per specimen. The previous series of 123 consecutive PNKB (Group II) showed gross haematuria (8.4%; P < 0.01 vs Group I) and symptomatic subcapsular haematoma (3.7%) with an adequate sampling of 94.8% (P < 0.01 vs Group I) and a mean glomerular count of 17 (range 4-47) per specimen (P < 0.01 vs Group I). Conclusions. PNKB is an invasive procedure that in spite of progress made in safety, diagnostic adequacy and performing techniques, still involves minor or major risks. The results obtained show that our method is extremely useful to reduce significantly the incidence of bleeding complications and permits us to take enough renal tissue for diagnostic evaluation in all cases.

Metabolic risk factors and markers of cardiovascular and renal damage in overweight subjects.

BACKGROUND: The prevalence of overweight and obesity in the United States has dramatically increased. Obesity clusters with a variety of hemodynamic and metabolic disturbances that increase the risk of cardiovascular disease. In this study we evaluated whether overweight subjects with hypertension also manifest hemodynamic and metabolic abnormalities compared with individuals of normal weight. METHODS: In a cohort of 129 patients with essential hypertension we measured the relationship between body mass index (BMI), blood pressure (BP), insulin sensitivity, lipid profile, and markers of organ damage including thickness of the carotid artery (IMT) and urine albumin excretion (UAE). A total of 41 normotensive, age-matched, healthy individuals served as control subjects. RESULTS: Hypertensive individuals showed higher levels of serum triglycerides, insulin area-under-the-curve (AUC), UAE, and greater IMT than normotensive subjects. Overweight hypertensive subjects showed higher levels of serum triglycerides, LDL cholesterol, glucose AUC, insulin AUC, UAE, and IMT than hypertensive subjects with normal body weight (BMI <25). Night-time systolic BP was higher and night-time fall in BP was lower among overweight than among normal-weight hypertensive patients. Simple regression analysis showed that BMI was correlated with age, UAE, BP, insulin and glucose AUC, serum triglycerides, cholesterol, and IMT in hypertensive subjects. However multiple regression analyses showed that BMI significantly correlated only with UAE. CONCLUSIONS: The study results show that increased body weight clusters with a variety of hemodynamic and metabolic abnormalities in hypertensive subjects. However multiple regression analyses showed a significant correlation only between BMI and UAE, a marker and predictor of cardiovascular and renal disease.

Renal flares in 91 SLE patients with diffuse proliferative glomerulonephritis.

BACKGROUND: Even when treated with current protocols, 25 to 30% of systemic lupus erythematosus (SLE) patients with diffuse proliferative glomerulonephritis (DPGN) evolve to end-stage renal disease (ESRD). The occurrence of renal flares is considered to be an important risk factor for the evolution to ESRD. The aim of this retrospective study was to evaluate the incidence and prognostic significance of renal flares in SLE patients with DPGN and to identify predictors for the occurrence of flares. METHODS: Ninety-one SLE patients were selected for study based on the following criteria: (a) evidence of renal involvement, (b) a follow-up of at least 6 months after the renal biopsy, and (c) a steady improvement in renal manifestations after the biopsy lasting for at least three months. RESULTS: Renal flares occurred in 54% of the patients after renal biopsy and appropriate treatment. A younger age at the time of renal biopsy correlated with the occurrence of renal flares. A high activity index (> or =10) and karyorrhexis on histology correlated with the occurrence of nephritic flares. Twenty-seven percent of the patients developed ESRD. The number of renal flares, nephritic flares, and "early" proteinuric flares (that is, those occurring in the first 18 months after renal biopsy) as well as serum creatinine levels, karyorrhexis, and chronicity index on renal histology were correlated with doubling serum creatinine. CONCLUSIONS: Our results suggest that (a) a distinct subgroup of SLE patients exists, made up of younger patients with extensive, active lesions on renal biopsy, who are at higher risk for renal flares, (b) renal flares represent important predictors of doubling serum creatinine.