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PubMed2002

Effects of short- and long-term lithium treatment on kidney functioning in patients with bipolar mood disorder.

Lithium (Li) carbonate has been reported to be able to cause some reversible functional changes in the kidney. In this study, the authors aimed to investigate whether the duration of Li treatment is the primary determinant of the changes in renal functioning due to the Li treatment. For this purpose, 10 Li-naïve (mean age+/-S.D.: 34.50+/-4.85), 10 short-term (mean age+/-S.D.: 31.77+/-7.61) and 10 long-term (mean age+/-S.D.: 36.60+/-10.15) Li-treated bipolar patients were included in the study. Serum blood urea nitrogen (BUN) and creatinine, urine creatinine levels, creatinine clearance, urine osmolality before and after 8-h water deprivation and urine osmolality after desmopressin injection were measured in all patients. Serum BUN and creatinine levels were within the normal limits and not statistically different among the groups. Creatinine clearance of the long-term Li-treated group was significantly lower than both that of the Li-naïve group and that of the short-term Li-treated group. After 8-h water deprivation and also after desmopressin injection, no difference was found among the groups in terms of urine osmolality. However, when each patient was evaluated individually in terms of their renal concentrating ability, partial nephrogenic diabetes insipidus was diagnosed in four patients on long-term and in two patients on short-term Li treatment. To our surprise, hypothalamic diabetes insipidus was also diagnosed in other two patients on long-term Li treatment. These results demonstrate that long-term Li treatment may cause impairment in renal concentrating ability, some of which may originate from the effects of Li on vasopressin on hypothalamic level, and a decrease in glomerular filtration rate (GFR). In the light of these data, we can conclude that long-term administration of Li may be a risk factor for Li-induced renal impairment, which is a progressive effect in nature.

Adult↗
PubMed2003

Why is erythropoietin made in the kidney? The kidney functions as a 'critmeter' to regulate the hematocrit.

The normal hematocrit is not a random number, but one that maximizes oxygen delivery. While the feedback loop wherein tissue oxygen pressure determines the production of erythropoietin, which further drives the production of red blood cells in the bone marrow, explains how the hematocrit is generated, it does not speak to how the hematocrit is regulated. The regulation of the hematocrit requires the coordination of the plasma volume and the red cell mass. By controlling red cell mass via erythropoietin and plasma volume through excretion of salt and water, the kidney is able to generate the hematocrit. It is hypothesized that the kidney functions as a critmeter by sensing the relative volumes of each component of the blood through the common signal of tissue oxygen tension. The kidney's unique ability to sense ECF volume through tissue oxygen signal allows it to coordinate these two volumes to produce the normal hematocrit. Hence, it may be the kidneys ability to report a measure of ECF volume as a tissue oxygen signal and thus to regulate the hematocrit that establishes it as the logical site of erythropoietin production. The critmeter is proposed to be a functional unit located at the tip of the cortical labyrinth at the juxta-medullary region of the kidney where erythropoietin is made physiologically. Renal vasculature and nephron segment heterogeneity in sodium reabsorption likely provides the anatomical construct to generate the marginal tissue oxygen pressure required to trigger the production of erythropoietin. The balance of oxygen consumption for sodium reabsorption and oxygen delivery is reflected by the tissue oxygen pressure. This balance hence determines RBC mass adjusted to plasma volume. Factors that affect blood supply and sodium reabsorption in a discordant manner may modulate the critmeter, e.g. angiotensin II. The objective of this work is to describe the hypothesis of the kidney's function as a critmeter, including the anatomical and physiological components, and the role of the renin-angiotensin system in modulating erythropoietin. Clinical examples of the dysregulation of the critmeter may be found in the anemia of renal failure and in sports anemia.

Anemia↗
PubMed1993

The effect of dorsomedial hypothalamic nucleus lesions on kidney function and structure after 1 and 12 months.

According to the Dillman theory (17), aging results from a deterioration of metabolism that begins with an elevation of hypothalamic receptor thresholds for feedback signals from the periphery. Three hypothalamic areas are known to contain such receptors: the ventromedial and dorsomedial hypothalamic nuclei (DMN) and the lateral hypothalamic area. We have hypothesized that selective destruction of those hypothalamic areas might be followed by physiological changes associated with aging. Electrolytic bilateral DMN lesions were produced in male and female weanling rats. These rats were maintained for up to 13 months of age. Sham-operated rats served as controls. Food intake and body weight were monitored postoperatively and prior to sacrifice. Before sacrifice, tail blood and a 24-h urine samples were obtained. In accordance with previous findings, rats with DMN lesions showed dramatic reductions of ponderal growth and food intake but had normal body composition. Total protein and albumin excretion rates were significantly lower in rats with lesions. The fractional contribution of albumin to total urinary protein was also decreased in rats with lesions. Histological examination of the kidneys showed significantly less pathology in the kidneys of rats with DMN lesions; the severity of renal pathology was correlated directly with proteinuria. These changes were seen as early as 1 month after production of the lesion. The attenuation of age-related changes in kidney functions and structure in rats with lesions could be due to reduced food intake (dietary restriction is known to produce similar results), and/or a direct effect of the lesion.(ABSTRACT TRUNCATED AT 250 WORDS)

Afferent Pathways↗
PubMed1995

Effects of cicletanine on kidney function. 1. Clearance and micropuncture studies in anesthetized rats.

The purpose of our study was to analyze the effect of cicletanine on kidney function by using clearance and free flow micropuncture techniques in anesthetized rats. In the clearance experiments, cicletanine was tested at three different doses (15, 30 and 60 mg/kg i.v.). The drug dose-dependently increased urine flow, and urinary sodium and chloride excretion. Renal potassium excretion was also significantly enhanced. Cicletanine was as effective as hydrochlorothiazide regarding fractional renal sodium excretion. Mean arterial blood pressure fell after cicletanine at doses of 30 and 60 mg/kg, but at none of the three doses tested did cicletanine affect renal plasma flow and glomerular filtration rate. In this regard it differed from hydrochlorothiazide which was found to markedly decrease glomerular filtration rate at a dose of 10 mg/kg i.v. A coadministration of cicletanine (20 mg/kg i.v.) and hydrochlorothiazide, at a maximal effective dose (20 mg/kg i.v.), induced an additional diuretic and saluretic effect. By puncturing of late proximal, early and late distal nephron segments, an action of cicletanine (30 mg/kg i.v.) in the superficial distal tubule could be established. Thus, cicletanine shares with the thiazide diuretics its tubular site of action despite the disparity in chemical structure between these drugs.

Animals↗
PubMed2002

Concomitance of diabetic retinopathy and proteinuria accelerates the rate of decline of kidney function in type 2 diabetic patients.

OBJECTIVE: To evaluate the rate of progression of renal disease in proteinuric type 2 diabetic patients with and without retinopathy. RESEARCH DESIGN AND METHODS: Thirty-eight proteinuric type 2 diabetic patients with diabetic retinopathy and 27 without were enrolled in an observational study for the evaluation of rate of glomerular filtration rate (GFR) decline and followed up for a median period of 6 years. GFR was determined at least once per year, and blood pressure, glycated hemoglobin, and proteinuria were determined every 4 months. RESULTS: Although the two groups had comparable GFR, albuminuria, blood pressure, and HbA(1c) at entry of the study, the rate of decline of GFR was higher in type 2 diabetic patients with retinopathy (-6.5 +/- 4.4 ml/year) than in those without (-1.8 +/- 4.8 ml/year; P < 0.0001). Protein and albumin excretion rate increased significantly in patients with retinopathy, while they did not change in those without. Mean blood pressure between the two groups of patients were similar both at entry and during the follow-up, although the proportion of patients treated with at least two antihypertensive drugs was higher in patients with retinopathy. On a multiple regression analysis, only mean blood pressure and proteinuria were significant determinants of progression of renal disease in type 2 diabetic patients with retinopathy. CONCLUSIONS: The rate of progression of renal disease in proteinuric type 2 diabetic patients with retinopathy is faster than that observed in those without retinopathy. The screening for retinopathy identifies patients at high risk for rapid deterioration of kidney function.

Albuminuria↗
PubMed2003

The effect of pneumoperitoneum on kidney function in laparoscopic donor nephrectomy.

Between June 1999 and November 2001 a prospective study was conducted to evaluate the effects of pneumoperitoneum during laparoscopic donor nephrectomy on kidney function using two different pressure settings (15 and 10 mm Hg). The effects were evaluated in both the donor's remaining kidney and the procured kidney in the recipient. There was no statistical significant difference in donors and recipients in regard to age, gender, and body mass index. In the two donor groups there was no difference in operative time (2.77 +/- 0.51 vs 2.70 +/- 0.52 hours; P = 0.579), intraoperative fluid (16.53 +/- 4.72 vs 19.54 +/- 7.04, P = 0.056), and urine output (1.81 +/- 0.53 vs 1.75 +/- 0.96 mL/kg/hour, P = 0.782) respectively. Donors' preoperative and first-day postoperative serum creatinine concentrations also did not differ for the groups (preoperative 0.87 +/- 0.21 vs 0.88 +/- 0.17 mg/dL; and postoperative 1.44 +/- 0.32 vs 1.38 +/- 0.29 mg dL, respectively; P = 0.696). Recipients' preoperative and postoperative serum creatinine concentrations on days 1, 2, 3, 7, 14, and 30 differed over time (P < 0.001) but not between groups (P = 0.541). We conclude that procurement of kidneys under either 10 or 15 mm Hg abdominal pressure gives equally good intraoperative and postoperative results.

Adult↗
PubMed1987

Deterioration of kidney function by high doses of co-trimoxazole in man.

High doses of co-trimoxazole in a patient with Pneumocystis carinii and impaired kidney function (creatinine clearance 10 ml/min) resulted in a declining renal clearance of the drug but did not affect the average creatinine clearance. The renal clearance of sulfamethoxazole and its metabolites 5-hydroxy-, N4-acetyl-, N4-acetyl-5-hydroxysulfamethoxazole decreased 80%, while the renal clearance of trimethoprim decreased 60%. The renal clearance of all compounds was evidently dependent on urine flow. The observed phenomena may be explained by the assumption that crystalluria occurred, obstructing kidney tubules. The crystalluria effect can be reversed by cessation of the drug or by lowering its dosage.

Adult↗
PubMed2000

Quantitative assessment of rat kidney function by measuring the clearance of the contrast agent Gd(DOTA) using dynamic MRI.

Magnetic resonance imaging (MRI) has been applied to assess kidney function in normal rats by monitoring the passage of the extracellular contrast agent GdDOTA. High-resolution images have been obtained using either the rapid acquisition with relaxation enhancement (RARE) or the snapshot pulse sequence. The latter was superior in anatomic definition due to the shorter echo delays used. The GdDOTA induced signal enhancements in the various renal structures were theoretically modeled and the results of the regression analysis then used to estimate local tissue concentrations in renal cortex, inner medulla and outer medulla/pelvis. The concentration-time curves in vena cava and renal cortex were similar and distinctly different from the ones in medulla and pelvis. This is reflected in the time-to-peak (TTP) values, which were TTP (blood) = 0.18 +/- 0.03 < TTP (cortex) = 0.26 +/- 0.05 < TTP (outer medulla) = 0.62 +/- 0.03 < TTP (inner medulla/pelvis) = 0.92 +/- 0.16 min. The initial tracer uptake rates depended linearly on the dose of GdDOTA administered, the value of the uptake rate in the cortex being significantly higher than those in the outer and inner medulla, which were identical within error limits. The initial medullar tracer uptake followed a first-order kinetics. The rate constant k(cl) = (dc[medulla]/dt)/c[cortex] = 3.4 +/- 0.5 min(-1) for the transition from cortex (predominantly blood signal) to medulla (predominantly urine) was considered a measure for the renal clearance. Intravenous administration of furosemide at doses 2.5, 5, and 10 mg/kg led to a dose-dependent decrease of k(cl). This reflects the inhibitory effect of the diuretic furosemide on medullary water resorption and thus the dilution of the GdDOTA in urine.

Animals↗
PubMed1993

The course of kidney function in type 2 (non-insulin-dependent) diabetic patients with diabetic nephropathy.

We evaluated the impact of some putative progression promoters on kidney function in albuminuric Type 2 (non-insulin-dependent) diabetic patients with biopsy-proven diabetic glomerulosclerosis. Twenty-six patients (1 female) with a mean age of 52 (standard error 2) years and a known mean duration of diabetes of 9 (1) years were followed-up prospectively for a mean of 5.2 (range 1.0-7.0) years. Twenty-one patients received antihypertensive treatment. During the observation period the glomerular filtration rate decreased from 83 (24-146) to 58 (2-145) ml.min-1 x 1.73 m-2 (mean (range)) (p < 0.001). The mean rate of decline in glomerular filtration rate was 5.7 (-3.5 to 22.0) ml/min per year. Albuminuria increased from 1.2 (0.3-7.2) to 2.3 (0.4-8.0) g/24 h (geometric mean (range)) (p < 0.001). Arterial blood pressure remained unchanged: 162/93 (SE 4/3) and 161/89 (4/2) mm Hg. Univariate analysis showed the rate of decline in glomerular filtration rate to correlate with systolic blood pressure (r = 0.71, p < 0.001), mean blood pressure (r = 0.56, p < 0.005), albuminuria (r = 0.58, p < 0.005) and the initial glomerular filtration rate (r = -0.49, p < 0.02). The rate of decline in glomerular filtration rate did not correlate significantly with dietary protein intake, total cholesterol, high-density lipoprotein cholesterol or HbA1c. Three patients died from uraemia and four patients died from cardiovascular disease. Two patients required renal replacement therapy at the end of the observation period. Our prospective observational study revealed that one-fifth of the patients developed end-stage renal failure during the 5-year observation period.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗