Serum hepatocyte growth factor levels in patients with chronic renal disease--effect of GFR and pathogenesis.

Hepatocyte growth factor (HGF) is a growth-promoting peptide that appears to act in a renotropic and nephroprotective manner during acute renal damage. Recent studies suggest that HGF is also of importance in chronic renal diseases. The serum HGF level is correlated with serum creatinine, and it has been suggested that glomerular and tubular diseases affect serum HGF differently. In the present study. levels of serum HGF were determined and correlated to glomerular filtration rate (GFR) in 118 patients with various chronic renal diseases. GFR was determined by 99mTc-DTPA clearance, and the GFR values were evenly distributed in the interval 5-155 mL/min/1.73 m2. Serum HGF levels increased slightly with decreasing GFR: the Pearson correlation coefficient being 0.49 (p<0.0001). In 21 additional patients with end-stage renal disease treated with continuous ambulatory peritoneal dialysis, there was a more marked increase in the serum levels of HGF. The effect of glomerular and tubular diseases on serum HGF was examined by comparing the HGF levels in two groups of patients with similar GFR values: 57 patients with mainly glomerular disorders (diabetic nephropathy with micro- or macroalbuminuria or glomerulonephritis) and 14 patients with mainly tubular disorders (polycystic kidney disease). There was no significant difference between the HGF levels of the two groups (p=0.30). In conclusion: Serum HGF levels are correlated with GFR (for GFR > or = 5 mL/min/1.73 m2) in patients with chronic renal diseases, and glomerular and tubular disorders seem to affect the HGF level similarly.     

Serum hepatocyte growth factor levels in patients with chronic renal disease - effect of GFR and pathogenesis

Hepatocyte growth factor (HGF) is a growth-promoting peptide that appears to act in a renotropic and nephroprotective manner during acute renal damage. Recent studies suggest that HGF is also of importance in chronic renal diseases. The serum HGF level is correlated with serum creatinine, and it has been suggested that glomerular and tubular diseases affect serum HGF differently. In the present study, levels of serum HGF were determined and correlated to glomerular filtration rate (GFR) in 118 patients with various chronic renal diseases. GFR was determined by 99m Tc-DTPA clearance, and the GFR values were evenly distributed in the interval 5-155 mL/min/1.73 m 2 . Serum HGF levels increased slightly with decreasing GFR; the Pearson correlation coefficient being 0.49 (p < 0.0001). In 21 additional patients with end-stage renal disease treated with continuous ambulatory peritoneal dialysis, there was a more marked increase in the serum levels of HGF. The effect of glomerular and tubular diseases on serum HGF was examined by comparing the HGF levels in two groups of patients with similar GFR values: 57 patients with mainly glomerular disorders (diabetic nephropathy with micro- or macroalbuminuria or glomerulonephritis) and 14 patients with mainly tubular disorders (polycystic kidney disease). There was no significant difference between the HGF levels of the two groups (p = 0.30). In conclusion: Serum HGF levels are correlated with GFR (for GFR &#85 5 mL/min/1.73 m 2 ) in patients with chronic renal diseases, and glomerular and tubular disorders seem to affect the HGF level similarly.     

水化治疗预防不同肾功能水平病人造影剂相关肾损伤的临床观察

[目的]探讨水化治疗预防不同肾小球滤过率（GFR）病人行冠状动脉介入术后造影剂相关肾损伤的效果,以便指导临床工作。[方法]将血肌酐正常的冠状动脉介入术后139例病人,根据GFR不同分为正常组和异常组,两组病人术后行常规水化治疗。比较两组术前、术后血肌酐、肾小球滤过率、血尿素氮、血清β2-微球蛋白、尿微量白蛋白、24 h出入量情况。[结果]两组术后均未发生造影剂肾病,术后6 h、12 h尿量差异有统计学意义（P〈0.05）;两组血尿素氮、β2-微球蛋白水平比较差异有统计学意义（P〈0.05）;术后第2天尿微量白蛋白与术前差值比较,差异有统计学意义（P〈0.05）。[结论]血肌酐正常的病人中有一部分潜在或已存在肾功能异常,术前应常规计算肾小球滤过率,临床可通过加强水化治疗预防不同肾小球滤过率的冠状动脉介入术后病人造影剂相关肾损伤。     

Cystatin C and estimates of renal function: searching for a better measure of kidney function in diabetic patients

BACKGROUND: Early identification of impairment in renal function is crucial in diabetic patients. Serum cystatin C may be the most sensitive indicator of glomerular filtration rate (GFR) in the clinical setting. METHODS: We compared cystatin C with creatinine, the Cockcroft-Gault (C-G) formula, and the Modification of Diet in Renal Disease (MDRD) study equation for the assessment of early decreased renal function in 288 diabetic patients (125 type 1, 163 type 2) with renal impairment [GFR: 4-222 mL x min(-1) x (1.73 m(2))(-1)]. Relationships of cystatin C, creatinine, and iohexol clearance were linearized by plotting their reciprocals in a simple regression model. Diagnostic efficiency was calculated from ROC curves. RESULTS: In this study population, cystatin C (P = 0.0013) was better correlated with GFR (r = 0.857) than were creatinine (r = 0.772), C-G (r = 0.750), and MDRD (r = 0.806), a result replicated in patients with normal renal function (P = 0.023, type 1; P = 0.011, type 2), but not in those with decreased GFR. Mean cystatin C concentrations showed step-by-step statistically significant increases as GFR decreased, allowing very early detection of reduction in renal function. At 90 mL x min(-1) x (1.73 m(2))(-1) and 75 mL x min(-1) x (1.73 m(2))(-1) cut-points, diagnostic efficiencies of cystatin C (89% and 92%) were better than those of the other variables (79%-82% and 85%-86%, respectively; P = 0.01). CONCLUSIONS: All data supported the value of serum cystatin C compared with conventional estimates based on serum creatinine measurement for detecting very early reduction of renal function. Use of cystatin C to measure renal function will optimize early detection, prevention, and treatment strategies for diabetic nephropathy.     

胱抑素C在2型糖尿病不同肾损害期的变化

目的探讨血清胱抑素C（Cysc）在2型糖尿病不同肾损害期的变化,评价Cys—C在2型糖尿病肾病早期的诊断价值。方法用颗粒增强免疫比浊法检测135例2型糖尿病患者（其中合并糖尿病肾病不同损害期77例）血清CysC,同时检测尿微量白蛋白排泄率（UAER）,血Alb、Cr、BUN,根据MDRD公式计算肾小球滤过率。结果2型糖尿病正常向蛋白尿组与2型糖尿病微量白蛋白尿组间Cys—C水平差异有统计学意义（P〈0．05,）;2型椿尿病微量白蛋白尿组与2型槠尿病人量白蛋白尿组间Cys—C水平差异有统计学意义（P〈0．01）。结论血清CysC可作为辅助2型糖尿病肾病早期诊断的指标。     

Beta 2-microglobulin concentration in plasma and production in liver cirrhosis

The beta 2-microglobulin plasma level is often high in patients suffering from cirrhosis. Many authors believe this to be due to an increased production, provided that the creatinine level is in the normal range. In the present study, alterations in the plasma level and production of beta 2-microglobulin were investigated in patients with liver cirrhosis without overt renal failure. 62 patients, 48 men and 14 women, suffering from liver cirrhosis were examined. The glomerular filtration rate (GFR) and plasma beta 2-microglobulin were measured in all patients and in 16 controls. As beta 2-microglobulin is freely filtered by glomeruli and its extrarenal catabolism is negligible, the beta 2-microglobulin filtration rate was calculated as the product of the beta 2-microglobulin plasma level times the GFR. In steady state conditions, the beta 2-microglobulin filtration rate may be used as an indirect index of beta 2-microglobulin production. The beta 2-microglobulin plasma level was high in 26 patients; however, only 12 of them showed a definite rise in beta 2-microglobulin production, as shown by an increased beta 2-microglobulin filtration rate. The 14 patients with high beta 2-microglobulin plasma levels without high beta 2-microglobulin filtration rates obviously showed a decreased GFR; however, creatinine was not increased because of its small sensitivity as an index of renal function. A linear correlation was found between IgG and the beta 2-microglobulin filtration rate (r = 052; p less than 0.02), not between IgG and the beta 2-microglobulin plasma level. The other indices of liver damage were not related to the beta 2-microglobulin filtration rate of plasma level.     

Serum cystatin C assay for the detection of early renal impairment in diabetic patients

The ability to assess renal function in diabetes patients rapidly and early is of major importance. This study was designed to determine whether cystatin C can replace serum creatinine as the screening marker for reduced glomerular filtration rate (GFR) in type 2 diabetes patients. The study was performed on 51 type 2 diabetic patients. GFR was estimated by the plasma clearance of (99m)Tc-DTPA. The correlation between (99m)Tc-DTPA clearance and levels of serum cystatin C, serum creatinine, and creatinine clearance was determined. Sensitivity and specificity for the diagnosis of renal impairment (defined as GFR<68 ml/min) were calculated by a receiver operating characteristic (ROC) curve for serum cystatin C, serum creatinine, and creatinine clearance. The correlation coefficients with (99m)Tc-DTPA clearance were -0.744 for serum cystatin C, -0.658 for serum creatinine, and +0.625 for creatinine clearance (P<0.001). With a cutoff value of 68 mL/min, the area under the ROC curve (AUC) was 0.891 for cystatin C, 0.77 for creatinine, and 0.753 for creatinine clearance. The AUC was statistically different between serum cystatin C and creatinine clearance (P<0.05). The ROC plot indicates that cystatin C is superior to serum creatinine and creatinine clearance for detecting impaired GFR. Serum cystatin C appropriately reflects GFR in diabetes, and is more efficacious than serum creatinine and creatinine clearance in detecting reduced GFR in type 2 diabetes patients.     

Evaluation of serum cystatin C and chromogranin A as markers of nephropathy in patients with type 2 diabetes mellitus

Nephropathy is a significant cause of morbidity and mortality in patients with diabetes mellitus (DM). The condition is characterized by persistent albuminuria and years of progressive renal structural changes associated with decline in the glomerular filtration rate (GFR). This study evaluates whether serum concentrations of the endogenous markers of GFR, cystatin C and chromogranin A could be used as indicators of nephropathy in 77 patients with Type 2 DM. On the basis of early morning urine microalbumin:creatinine ratio, patients were divided into patients without diabetic nephropathy (DN) who were normoalbuminuric (n = 27) and patients with DN who were microalbuminuric (n = 8) or macroalbuminuric (n = 42). Patients with reduced GFR or elevated serum cystatin C did not show the expected increase in serum chromogranin A. Twenty-six percent of the patients with normoalbuminuria and 6% of those with DN had serum chromogranin A below the detection limit of the assay (< 2 U/L). In patients with DN, serum chromogranin A showed significant correlation with serum cystatin C, but not with serum creatinine and creatinine clearance. Serum cystatin C and creatinine showed poor correlation with duration of DM and HbA1c. Serum cystatin C and creatinine were significantly higher in patients with DN than in normoalbuminuric patients. Serum cystatin C showed significant correlation with serum creatinine (rs = 0.45, p = 0.002), but not with creatinine clearance (rs = 0.23, p = 0.17) in patients with DN. Four of nine patients with creatinine clearance between 50 and 80 mL/min had increased (> or = 1.4 mg/L) serum cystatin C compared with only two patients with increased serum creatinine concentration. Twenty of 50 (40%) patients with DN had elevated serum cystatin C compared with 6 of 50 (12%) with elevated serum creatinine. If microalbuminuria is regarded as the "gold-standard" test, serum cystatin C has a sensitivity of 40% and specificity of 100% for the detection of DN. However, further studies are required to confirm the usefulness of serum cystatin C estimation as a screening test and as an early indicator and predictor of the development of DN.     

Serum laminin P1 fragment concentration in renal diseases

The serum concentration of laminin P1 fragment was determined in various histologically proven renal diseases by a competitive radioimmunoassay directed against the pepsin-resistant fragment P1. The serum laminin P1 fragment level of healthy subjects (n = 71) was 1.35 +/- 0.19 U/ml. Serum levels of laminin P1 fragment in patients with minimal change nephrosis in the remission phase and those with IgA nephropathy showed no significant difference when compared with healthy controls. However, patients with minimal change nephrosis in the nephrotic phase, membranous glomerulonephritis, diabetic nephropathy, lupus nephritis and renal cell carcinoma showed significantly higher levels (P less than 0.01) of serum laminin P1 fragment. No correlation was observed between serum laminin P1 fragment level and creatinine clearance. These results suggest that changes in serum laminin P1 fragment level could be used to indicate alterations in glomerular basement membrane metabolism in renal disease.     

Urinary excretion of complement C3d in patients with renal diseases

INTRODUCTION: Complement-mediated tubular injury may play an important role in the progression of renal diseases. C3d is a presumed marker of complement activation. Its precursor C3dg has been detected in the urine of patients with membranous nephropathy. However, little is known of the renal handling of C3d or its excretion in other renal diseases. METHODS: We measured the urinary excretion of albumin, IgG, beta2-microglobulin (beta2m), and of complement C3d in patients with tubulo-interstitial nephritis (TIN; n= 8), in patients with membranous nephropathy (n = 35) and in patients with nonmembranous glomerular diseases (23 nonproliferative and 21 proliferative). Fractional excretions (FE) were calculated using creatinine clearance as marker of GFR. RESULTS: C3d was not measurable in the urine of the healthy controls, but was detectable in seven out of eight of the TIN patients (median excretion 0.11 mU min-1, range 0.006-2.4 mU min-1). In these patients the urinary excretion of beta2m was clearly elevated (median 26.6 micro g min-1, range 1.0-103 micro g min-1). The FE of C3d correlated with the FE of beta2microglobulin (r = 0.83, P = 0.01), and their ratio amounted to 0.03 (range 0.003-0.06), a value in agreement with the expected sieving coefficient. Urine C3d was detectable in all but three of the patients with glomerular diseases (median excretion 0.36 mU min-1, range 0.004-7.9 mU min-1); C3d-excretion did not differ between the three subgroups of patients with glomerular diseases. FEC3d correlated with FEIgG (r = 0.88, P < 0.01). The ratio FEC3d/FEbeta2m was 0.78 (range 0.04-9.99). Selected patients with membranous nephropathy were re-analyzed after (partial) remission of proteinuria. Reduction of proteinuria resulted in a decrease of C3d excretion. CONCLUSION: Urinary excretion of C3d is elevated in patients with TIN, most likely as a mere consequence of decreased tubular reabsorption. In patients with glomerular diseases urinary excretion of C3d is increased and related to proteinuria, independent of the underlying glomerular disease. In these patients there is evidence of increased local formation of C3d.     

Renal function--estimation of glomerular filtration rate.

Assessment and follow-up of renal dysfunction is important in the early detection and management of chronic kidney disease. The glomerular filtration rate (GFR) is the most accurate measurement of kidney disease and is reduced before the onset of clinical symptoms. Drawbacks to the measurement of GFR include the high cost and incompatibility with routine laboratory monitoring. Serum creatinine determination is a mainstay in the routine laboratory profile of renal function. The measurement of serum cystatin C has been proposed as a more sensitive marker for GFR. According to National Kidney Foundation-K/DOQ1 clinical guidelines for chronic kidney disease, serum markers should not be used alone to assess GFR. Based on prediction equations, clinical laboratories should report an estimate of GFR, in addition to reporting the serum value. In this article, information is presented on how best to estimate GFR using prediction equations for adults and for children. Using serum creatinine concentration with the Modification of Diet in Renal Disease (MDRD) study equation offers a suitable estimation of GFR in adults. The cystatin C prediction equation with the use of a prepubertal factor seems superior to creatinine-based prediction equations in children of <14 years.     

Pyrimethamine inhibits renal secretion of creatinine.

The mechanism of increased serum creatinine after administration of pyrimethamine and dapsone was evaluated for six healthy volunteers. Serum parameters, urine sediment, and clearances of creatinine, inulin, and para-aminohippurate were assessed prior to and 28 h after the ingestion of a single, combined dose of 100 mg of pyrimethamine and 200 mg of dapsone. In a second series, the same renal function tests were performed for nine human immunodeficiency virus-infected men before and after 1 month of prophylactic treatment with a weekly dose of 75 mg of pyrimethamine and 200 mg of dapsone to evaluate sustained effects on renal function. Serum creatinine increased within 28 h from 81 +/- 14 to 102 +/- 16 mumol/liter (P = 0.002) in the healthy volunteers. Blood urea nitrogen, beta 2-microglobulin, and urine remained normal. Creatinine clearance decreased from 125 +/- 27 to 91 +/- 26 ml/min (P < 0.02) without changes in inulin clearance. The effect was reversible within 21 days and attributable to pyrimethamine, as determined by administration of each drug alone. The sustained effect of four doses of pyrimethamine and dapsone in human immunodeficiency virus-infected patients consisted of an analogous rise in serum creatinine from 69 +/- 17 to 87 +/- 32 mumol/liter (P < 0.05). Both creatinine and inulin clearances, however, were unchanged, representing a new equilibrium between creatinine production and elimination at a higher level in serum. Pyrimethamine, thus, may reversibly inhibit renal tubular secretion of creatinine without affecting the glomerular filtration rate. This physiologic effect in pyrimethamine-treated patients must be differentiated from possible organ-related nephropathies.     

A 1-year follow-up study on the effect of atenolol on serum beta 2-microglobulin level in hypertensive diabetic patients

Hypertensive diabetic patients are particularly prone to renal function impairment. A total of nine out-patients with diabetes and hypertension were, therefore, entered into this single-blind uncontrolled study on the effects of 50 mg/day atenolol on reducing blood pressure and preserving normal kidney functioning. Treatment and evaluations were continued for 12 months. Serum beta 2-microglobulin concentration was used as the index for measuring renal impairment. Atenolol significantly reduced heart rate, systolic and diastolic blood pressure, and serum beta 2-microglobulin concentrations compared with baseline. Plasma glucose and glycosylated haemoglobin levels were unchanged, and blood urea nitrogen levels were increased slightly (non-significant). Serum creatinine showed a tendency (non-significant) to reflect the changes in beta 2-microglobulin concentration. Ways in which atenolol may act to improve kidney functioning are suggested. It is concluded that atenolol is a favourable choice for the treatment of hypertension in diabetic patients with normally functioning kidneys since, even in long-term use, normal renal functioning is preserved.     

Lipid metabolism and functional status of the kidney in hypothyroid patients depending on the phase of disease

AIM: To evaluate renal function in correlation with lipid metabolism parameters in patients with primary hypothyroidism (HT) in compensation and decompensation. MATERIAL AND METHODS: 45 HT patients' examination included study of blood creatinine, urea, cholesterol, triglycerides, high and low density lipoproteins, urinary microalbumin, thyroid hormones and thyrotropin, beta 2-microglobulin levels, glomerular filtration rate (GFR), renal functional reserve (RFR). Also, Zimnitsky test and ultrasound investigation of the kidneys were made. RESULTS: It was found that renal dysfunction in decompensated HT is characterized by normal renal concentration function, high intraglomerular pressure (low GFR and RFR), high concentration of beta 2-microglobulin in blood. Severe HT runs with negative correlation between GFR and total blood cholesterol, LDL. Albuminuria and low RFR in decompensated HT and marked hyperlipidemia suggest development of glomerulopathy related to abnormal physicochemical processes in glomerular endothelium. CONCLUSION: Patients with decompensated HT have apparant glomerular dysfunction and disturbances in lipid metabolism. Hyperlipidemia in HT is a factor of renal damage.     

胱抑素C及同型半胱氨酸的血清含量与糖尿病肾病患者肾小球滤过率的相关性研究

目的:通过检测血胱抑素C(CystatinC,CysC)、同型半胱氨酸(Homocysteine,Hcy)浓度及尿白蛋白清除率(urinealbumin excretionrate,UAER)在糖尿病肾病(diabetic nephropathy,DN)进程中的变化以及与肾小球滤过率(glomerular filtration rate,GFR)的相关性,探讨其在DN诊断中的价值。方法:共47例患者,根据肾小球滤过率将其分为早期糖尿病肾病组(early-DN组,GFR≥60mL/min)及晚期糖尿病肾病组(end-DN组,GFR<60mL/min),比较两组间CysC、Hcy的变化以及与肾小球滤过率的相关性。结果:end-DN组CysC、UAER均高于early-DN组(P<0.01)。相关分析显示肾小球滤过率与CysC、Hcy、UAER负相关(r=-0.584,P=0.000;r=-0.547,P=0.000;r=-0.507,P=0.000),在慢性肾脏病(chronic kidney disease,CKD)Ⅱ、Ⅲ期,肾小球滤过率与CysC、Hcy负相关(r=-0.617,P=0.000;r=-0.431,P=0.018)。结论:糖尿病患者中,伴随慢性肾脏病进程,CysC、Hcy、UAER逐渐升高,尤其在CKDⅡ、Ⅲ期,CysC、Hcy联合检测与UAER比较,能更好的反应糖尿病肾病肾小球滤过功能异常。     

Analysis of glomerular filtration rate, serum cystatin C levels, and renal resistive index values in cirrhosis patients.

BACKGROUND: The aim of this study was to evaluate the relation of glomerular filtration rate (GFR) to serum cystatin C levels, renal resistive index (RRI), serum creatinine and creatinine clearance in patients with different stages of cirrhosis. METHODS: The study sample was 25 cirrhotic patients (10 females and 15 males; mean age 57.3+/-2.04 years), 10 in the compensated stage without ascites and 15 in the decompensated stage with new-onset ascites. None had azotemia nor were on diuretic treatment. The control group comprised 25 healthy adults (11 female and 14 men; mean age 56.56+/-1.91 years). Serum cystatin C, RRI, serum creatinine and creatinine clearance were measured. GFR was determined by technetium(99m)-diethylene triamine pentaacetic acid renal scintigraphy. RESULTS: Cirrhosis cases had lower mean scintigraphic GFR than controls (64.5+/-4.03 vs. 87.96+/-4.16 mL/min, p<0.05). Serum cystatin C and RRI were significantly higher in the cirrhotic group compared to controls (1.16+/-0.09 mg/L and 0.68+/-0.01 vs. 0.86+/-0.03 mg/L and 0.64+/-0.01, respectively; p<0.05). Subgroup comparative analysis showed that only two parameters, scintigraphic GFR and serum cystatin C, were significantly different between compensated and decompensated cirrhotics (75.62+/-4.9 mL/min and 0.89+/-0.07 mg/L vs. 57.23+/-5.14 mL/min and 1.34+/-0.13 mg/L, respectively; p<0.05). Scintigraphic GFR showed significant correlation with cystatin C, but not with serum creatinine or creatinine clearance (r=-0.877, p<0.05) in decompensated patients. No correlation was observed between scintigraphic GFR and RRI or between serum cystatin C and RRI in all subjects. A receiver operator characteristics curve showed that cystatin C at a cutoff value of 1.01 mg/L can significantly differentiate patients with GFR <70 mL/min with 80% sensitivity and 80% specificity. CONCLUSIONS: Serum cystatin C, but not serum creatinine or RRI measurement, correlates with GFR in each stage of liver failure and has a significant diagnostic advantage in detecting lower GFR in such cases.     

ACE gene polymorphism as a prognostic indicator in patients with type 2 diabetes and established renal disease.

OBJECTIVE: To investigate whether the DD genotype is a predictor of mortality and of the decline in renal function in patients with type 2 diabetes and established nephropathy. RESEARCH DESIGN AND METHODS: A total of 56 such patients of Maltese Caucasian descent were recruited, and their ACE genotype was determined. Serum creatinine was estimated approximately every 4 months. The glomerular filtration rate (GFR) was calculated according to the Cockroft-Gault formula, and rate of change was determined by regression analysis. RESULTS: The rate of change in calculated GFR was -7.76 ml.min(-1).year(-1) in those with the DD genotype (n = 31) and -1.17 ml. min(-1). h(-1) in those with the ID or II genotype (n = 25) (P < 0.01). The 3-year mortality was 45.2% in the DD group compared with 20.0% in the ID/II group (P < 0.05). CONCLUSIONS: The DD genotype of the ACE gene polymorphism is associated with a more rapid decline in renal function and higher mortality in type 2 diabetic patients with established nephropathy.     

The blood serum concentration of cystatin C (gamma-trace) as a measure of the glomerular filtration rate

The blood serum concentrations of creatinine and the low molecular weight proteins cystatin C, beta 2-microglobulin and retinol-binding protein were measured in 106 patients whose glomerular filtration rates were assessed by Cr-ethylenediaminetetraacetate (EDTA)-clearance determinations. The reciprocals of the serum concentrations of creatinine, cystatin C and beta 2-microglobulin were closely correlated to the Cr-EDTA-clearance (r = 0.73, 0.75 and 0.70, respectively) in contrast to the corresponding values for retinol-binding protein (r = 0.39). The calculated values of the glomerular elimination rate for creatinine and cystatin C were normally distributed in contrast to those for beta 2-microglobulin. The calculated glomerular elimination rate of cystatin C was not correlated to age, sex, type of disorder or disease activity. The results demonstrate that the serum level of cystatin C is a better measure of the glomerular filtration rate than the serum level of beta 2-microglobulin.     

Assessment of renal function: selected developments

Tests commonly used to assess the glomerular filtration rate (GFR) and to detect renal tubular damage are critically reviewed. Creatinine clearance which is frequently used for assessment of the GFR is prone to several errors. The plasma creatinine can be used to provide a rough guide but for reliable measurement of the GFR, 51Cr-EDTA clearance is recommended. Measurements of the urinary excretion of low molecular weight proteins, enzymes and kidney tissue proteins have been used to detect tubular damage. Of the low molecular weight proteins excreted, beta-2-microglobulin is unstable and measurement of retinol-binding protein or alpha-1-microglobulin is recommended for the detection of chronic renal tubular malfunction. Of the many enzymes that have been studied, urinary N-acetyl-beta-D-glucosaminidase or alanine aminopeptidase are recommended as being the most useful for the early detection of acute renal tubular damage. Among renal tissue proteins that have been measured in urine adenosine-deaminase-binding protein, a tubular brush border antigen appears to have considerable potential for providing early warning of renal allograft rejection.     

简化肾脏病膳食改善方程在慢性肾脏病诊断及治疗中的应用

目的通过检测患者肾小球滤过率（GFR）了解住院患者的肾功能及肾脏损害程度。应用简化肾脏病膳食改善（MDRD）方程估算GFR,为临床选择药物及用药量提供更可靠的依据。方法通过统计8 940例住院成年患者的基本信息,按照性别、年龄、疾病的不同类型及血肌酐水平进行分组。利用MDRD方程估算出患者的GFR。肾损害程度分期采用美国肾病学会（NKF）2002年的慢性肾脏病（CKD）分期。结果8 940例患者中,40.1%的患者存在肾功能不全（GFR〈90 mL/min）,32.1%的患者存在隐匿性肾功能不全（血肌酐〈106μmol/L,GFR〈90 mL/min）。506例体检者中有15.2%存在隐匿性肾功能不全。结论由于住院患者多数存在肾功能受损情况,院外部分人群存在隐匿性肾功能不全的隐患,因此应用MDRD方程能更准确地估算GFR值,有利于临床医生在治疗中采用不同的治疗方案。