Use of α1-microglobulin for diagnosing chronic interstitial nephropathy.

α1-Microglobulin (α1M) is a low molecular weight protein and has been best characterized for detecting acute lesions of proximal tubules (Bonventre in Contrib Nephrol 156:213-219, 2007). This study has tried to evaluate the use of α1M for the differential diagnosis of chronic interstitial nephropathy. 145 patients were recruited [81 men and 64 women, mean age 61.8 ± 16.7 years, 64.8 % have an estimated glomerular filtration (GFR) <60 ml/min]. Urinary α1M was evaluated using an immunonephelometric assay. 82 patients were diagnosed as having chronic interstitial nephritis (CIN), and 46 patients have been previously diagnosed of glomerulonephritis (GN). A group of hypertensive patients without renal disease was used as control (n = 17). Patients in GN group had the highest α1M excretion (15.05 mg/24 h). When the α1M/albuminuria rates were calculated, the CIN group had the highest rate (1.03 mg/mg) and the GN group had the lowest rate (0.04 mg/mg) (p < 0.001). When the α1M/proteinuria rates were calculated, the results were rather similar. The AUC for CIN group was 0.785, and the one for GN group was 0.139. Patients with estimated GFR <60 ml/min showed a higher excretion of α1M (18.75, 8.75-40.00 mg/24 h). Nevertheless, α1M/albuminuria and α1M/proteinuria rates were still higher in CIN patients with GFR ≥60 ml/min. α1M urinary excretion is increased in chronic interstitial nephropathy and glomerulonephritis as well as in patients with GFR <60 ml/min. The α1M/albuminuria rate and the α1M/proteinuria quotient are increased in chronic interstitial nephropathies but decreased in glomerular diseases.

Hematocrit, urea and gender: the Hematocrit, Urea and GEnder formula for prognosing progressive renal failure in diabetic nephropathy.

OBJECTIVE: Diabetic nephropathy is a common cause of end stage renal disease. Notwithstanding, wide inter-individual variations in the speed of progression of diabetic nephropathy are frequent. We have used the score of the HUGE formula to predict progression of kidney disease in a group of diabetic nephropathy patients. DESIGN AND METHODS: The sample consisted of 84 type 2 diabetic patients. At treatment entry, the mean age was 62.1 ± 12.5 years and 59.5% were male. Blood pressure was measured at office at each visit. Serum creatinine, urea, hematocrit and 24h proteinuria were analyzed every 6 months. HUGE score was calculated from gender, urea and hematocrit. RESULTS: Mean HUGE score was 0.99 ± 3.88. Using as cut off point 1.5, those patients who had a score equal or higher (n=31) showed a bigger increase in serum creatinine after one year (41.8 ± 62.1%) than those subjects with score<1.5 (n=53) (18.7 ± 38.6%, p=0.041). 5 patients with low HUGE score reached end stage renal failure (9.4%) and 10 patients in the high HUGE score group (32.3, p=0.008). When logistic regression analysis was performed only a HUGE score higher than 1.5 (p=0.003) and proteinuria higher than 2g/day (p=0.041) were independently associated to CRF progression (creatinine increment>25%). CONCLUSIONS: In diabetic nephropathy patients the HUGE equation may be useful to detect the subjects prone to progressive renal failure. Wider samples will be needed to confirm this finding and, most important, its applicability to other kinds of nephropathy.

Angiotensin-converting enzyme inhibitors versus angiotensin receptor blockers for diabetic nephropathy: a retrospective comparison.

INTRODUCTION: There are no adequate head-to-head comparisons of angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB) in type 2 diabetic patients in spite of some interesting attempts. Furthermore, there are no adequate studies about the effects of ACE inhibitors in type 2 diabetic patients, who are the great majority of diabetic individuals. This study has retrospectively compared the effects of ACE inhibitors and ARBs used to treat diabetic nephropathy in a group of type 2 diabetic subjects. DESIGN AND METHODS: Patients (n=154) were treated with ACE inhibitors (mean age 59.5+/-13.3 years, 52.6% were male). Eighty-five patients had been treated with ARBs from 1999 until now (mean age 62.6+/-10.9 years, 56.0% were male, differences not significant). Kaplan-Meier survival analysis was used to calculate survival before reaching end-stage renal disease (ESRD) (glomerular filtration < 15 ml/min, stage V of renal disease as defined by KDOQI clinical guidelines) or starting renal replacement therapy. Only patients treated for more than six months were included in the survival analysis. Comparison of survival was made at three, five and seven years after starting treatment. RESULTS: Pre-ESRD survival was 91.9% at three years, 81.6% at five years and 61.9% at seven years of follow-up for patients treated with ACE inhibitors. For patients treated with ARBs, pre-ESRD survival was 95.3% at three years, 82.1% at five years and 78.2% at seven years of follow-up (p=0.02, log-rank test). At 36 months, the comparative odds ratio for having started renal replacement therapy or reaching end-stage renal failure was 0.246 (95% confidence interval 0.114-0.531, p<0.001 for chi-square and likelihood ratio tests). The risk for the ARB cohort was 0.682 (95% confidence interval 0.578-0.804), meanwhile for ACE inhibitor patients it was 2.768 (95% confidence interval 1.481-5.172). CONCLUSIONS: The effects of ACE inhibitors and ARBs seem to be different, favouring the use of ARBs. These results may have been influenced by the different circumstances when each kind of drug was indicated, since ARBs were used with the specific recommendations for control of blood pressure in diabetic patients. An earlier referral of these patients may also have had some effect on these results. The need for a well-designed prospective study on type 2 diabetic patients with heavy proteinuria is warranted.

Nighttime blood pressure fall in renal disease patients.

OBJECTIVE: There are controversial reports in the prevalence of abnormal nighttime blood pressure fall in renal patients. It has been evaluated nocturnal BP in renal patients using 24 h blood pressure monitoring (ABPM) in comparison with nontreated control subjects either normotensives or hypertensives. DESIGN AND METHODS: It has been reviewed 137 ABPM studies performed in renal patients (47.8 +/- 15.4 years, 76 men and 61 women). The control group includes 119 subjects without kidney disease, 65 were normotensives, and 49 were hypertensives, aged 46.8 +/- 12.1 years, 59 men and 60 women. The ambulatory BP was measured noninvasively for 24h by the SpaceLabs 90207 device programmed to measure BP every 15 min during daytime and every 20 min during nighttime. The definition of daytime and nighttime was made on the basis of wakefulness and sleep or bed rest periods, obtained from a diary kept by each subject. RESULTS: SBP, but not DBP, was higher (133.9/81.7) in renal disease patients when compared to nonrenal subjects (127.9/80.8, p < 0.01). When the control group was split into normotensive and hypertensive patients there were still significant differences, but hypertensives had higher BP than renal disease patients (139.0/89.7, p < 0.05). Nocturnal SBP fall in renal disease patients was reduced (5.8%, p < 0.001) and so was DBP fall (11.1%, p < 0.001) compared with the overall nonrenal patients sample (SBP 10.8; DBP 15.3%). The frequency of nondipper status in renal disease patients (39.6%) was higher than in control patients (18.4%, p < 0.001). Nontreated normotensive renal disease patients did not show any difference in either SBP or DBP nighttime fall with respect to control normotensives. Neither do nontreated hypertensive renal patients as compared with control hypertensives. There were not differences between proteinuric and nonproteinuric patients in nocturnal BP fall. The same result was obtained when hypertensive and normotensive nontreated renal patients were compared. The presence of renal failure did not induce a reduction of nocturnal BP fall. Most of treated renal patients were mainly receiving drug therapy during the morning and frequently this was the single daily dose. CONCLUSIONS: Altered diurnal rhythm should not be considered as a usual complication of renal disease. Inadequate antihypertensive pharmacotherapy could be related to the abnormalities of nighttime BP fall when it is detected.

Sympathetic skin response in peritoneal dialysis patients.

To determine if there is any difference in nerve conduction studies or sympathetic skin response (SSR) between patients on peritoneal dialysis and those on regular hemodialysis, we did a cross-sectional observational study. The study group consisted of 24 patients on peritoneal dialysis (PD) (12 men, aged 45 +/- 17 years) and 20 patients on hemodialysis (HD) (11 men, aged 50 +/- 22 years). All of these patients were in stable clinical condition, they were receiving adequate dialysis, and none of them had systemic diseases. Motor and sensory nerve conduction studies of the common and medial peroneal nerve and SSR were performed in all patients. There were no differences in motor and sensory nerve conduction velocities between PD and HD patients. All PD patients had detectable SSR. However, six patients on HD (30%) failed to show SSR (p < 0.05). Mean SSR amplitude was higher in PD patients than in HD patients (1233 +/- 843 vs. 605 +/- 771 microv, p < 0.05). There were no differences in mean SSR latency between PD and HD patients. PD modality (continuous ambulatory PD vs. automated PD) or the presence of residual renal function did not influence nerve conduction studies or SSR. In conclusion, using standard nerve conduction studies, no differences could be found between HD and PD. However, a higher proportion of patients on HD showed an impaired SSR, suggesting that subclinical neuropathy may be more common in HD than PD patients.