Urinary epidermal growth factor excretion in children with chronic renal failure.

To investigate the excretion of urinary epidermal growth factor (EGF) in children with chronic renal failure (CRF), we have measured the urinary EGF/creatinine ratio (EGF/Cr) and the 24-hour urine EGF concentration in 19 children with CRF, 11 children with kidney disease and normal creatinine clearance, and 12 healthy children. Children with CRF had a significantly lower daily urine EGF concentration as well as urinary EGF/Cr. In contrast, children with kidney disease and normal renal function had normal daily urine EGF levels and urinary EGF/Cr. Accompanied by no difference in serum EGF between these two groups of patients, these data provide indirect evidence of the kidney as a source of human urinary EGF. There was a positive correlation of urinary EGF/Cr with creatinine clearance in all renal patients (r = 0.608, n = 30, p < 0.001). A much better correlation was found between daily urine EGF and creatinine clearance (r = 0.855, n = 30, p < 0.001). Our results implicate that there is a functional relationship between glomerular filtration and urinary EGF excretion, and that the urinary EGF/Cr may be a reliable indicator of urinary EGF excretion in children with CRF.     

Urinary excretion of urodilatin in healthy children and children with renal disease

Urodilatin (URO) is a natriuretic peptide isolated from human urine which is thought to be produced by distal tubular cells. We measured urinary URO excretion in 50 healthy children and 23 children with acute (ARF), chronic renal failure (CRF), or hereditary tubular disorders, using a specific radioimmunoassay. The mean URO excreted in these four groups was 56, 45, 94, and 121 fmol/min per 1.73 m², respectively (differences between first three groups not significant). The variation in URO excretion was larger in patients with kidney disease than in controls. There were significant correlations between urinary URO and sodium excretion in controls and CRF, but not in ARF. URO excretion also correlated with urine flow rate in CRF. Although no correlation was found between URO excretion and creatinine clearance, urinary URO was increased in some patients with advanced CRF, which suggests stimulated tubular production to compensate for reduced sodium excretion. In view of the therapeutic potential of URO in renal insufficiency, further study of the renal handling of URO is warranted. Received December 4, 1996; received in revised form and accepted June 13, 1997     

内皮素在移植肾急性或慢性排斥反应中的变化

目的：探讨内皮素—1(ET—1)在移植肾急性或慢性排斥反应(简称急排或慢排)中的变化。方法：对43例肾移植术1年后患者(对照组18例，急排组9例，慢排组16例)行血液、尿液ET—1、肌酐、β2—M排泄量等测定，对部分急排和慢排移植肾行ET—1及A受体免疫组织化学染色。结果：急排组血、尿ET—1高于对照组(P＜0．01)；急排组尿ET—1明显高于慢排组(P＜0．01)，两组间血ET—1的差异无明显意义(P＞0．05)；急排和慢排时血ET—1均与血肌酐呈正相关(P＜0.01)，尿ET—1均与尿β2—M排泄量呈正相关(P＜0．01)；免疫组织化学染色显示ET—1与ETA受体在移植肾内的分布较一致，与相应病理类型大致吻合，急排和慢排检测时，其染色强度明显高于正常肾脏。结论：检测尿ET—1排泄量可鉴别急排和慢排，术后监测尿ET—1较监测血ET—1更有意义；在急排和慢排中ET系统可能担当重要角色。     

Urinary glycosaminoglycan excretion in healthy and stone-forming children

Both in vivo and in vitro studies suggest that macromolecules excreted in the urine, e. g. glycosaminoglycans (GAGs) may be inhibitors of kidney stone formation. We evaluated urinary GAG excretion in 22 children with calcium oxalate stones [8 with absorptive hypercalciuria, 6 with renal hypercalciuria (RH), 8 with normocalciuria], and in 20 age-matched controls. There was no significant difference between the two groups in the total urinary GAG level. In terms of the various GAG fractions, patients with RH excreted considerably less keratan sulphate and considerably more dermatan sulphate than the other patients and healthy controls. There was no difference between the two groups in condroitin sulphate, heparan sulphate and hyaluronic acid excretion. We conclude that there is no significant correlation between the formation of calcium oxalate stones and urinary GAG excretion. Received January 31, 1995; received in revised form and accepted February 6, 1996     

Factors affecting renal hydrogen ion excretion capacity in healthy children

In 560 healthy German children and adolescents aged 2.8–22.0 years from the DONALD (Dortmund Nutritional and Anthropometric Longitudinally Designed) study, the relationship between urine pH and renal net acid excretion (mmol/day/1.73 m²) was analysed. A quadratic model showed the best fit (r ²=0.608). Using logistic regression analysis three parameters (urinary phosphorus excretion, total protein intake and urinary ratio of potassium and sodium) had a significant effect on renal hydrogen ion excretion capacity characterised by the probability of high or low net acid excretion with respect to the urine pH value. Urinary osmolality, in contrast to what has been seen in a previous experimental study with low birth weight infants, along with sex and age had no significant independent effects on renal net acid excretion with respect to the urine pH value over the range of osmolalities observed. In healthy children and adolescents a low fluid intake with high urinary osmolality does not at least substantially decrease the renal capacity of hydrogen ion excretion. Received: 7 April 2000 / Revised: 15 December 2000 / Accepted: 15 December 2000     

Urinary excretion of endothelin-1 (ET-1), transforming growth factor- beta1 (TGF- beta1) and vascular endothelial growth factor (VEGF165) in paediatric chronic kidney diseases: results of the ESCAPE trial.

The severity and dynamics of renal tissue damage in chronic kidney disease (CKD) may be reflected by the urinary excretion of vasoactive and growth factors released by the damaged kidney. Urinary excretion of ET-1, TGF-beta1 and VEGF(165) was evaluated in 303 children with CKD stage II-IV (GFR 48 +/- 22 ml/min/1.73 m(2)) and 81 age-matched healthy controls. Major renal disease groups were hypo-/dysplastic kidney disease (N = 183), obstructive uropathies (N = 47), glomerulopathies (N = 34), nephronophthisis (N = 19) and polycystic kidney disease (N = 20). RESULTS: The mean urinary excretion rates of each of the three putative biomarkers were significantly elevated in CKD patients compared to controls: 965 +/- 2042 vs 216 +/- 335 fmol/g creatinine for ET-1; 252 +/- 338 vs 155 +/- 158 ng/g for VEGF; 31.6 +/- 37.0 vs 10.9 +/- 9.8 ng/g for TGF-beta1 (each P < 0.0001). The excretion of ET-1 and TGF-beta1 was highest in patients with obstructive uropathies. In the patients, ET-1, TGF-beta1 and VEGF excretion rates were inversely correlated with age (r = -0.22, -0.32 and -0.17, all P < 0.005) and renal function (r = -0.21, -0.13 and -0.15; P < 0.001; < 0.05; < 0.01; respectively) VEGF and TGF-beta1 excretion rates were positively correlated both in patients and controls. CONCLUSIONS: Children with CKD exhibit significantly elevated urinary excretion of ET-1, TGF-beta1 and VEGF(165) in comparison to healthy children. Urinary excretion of these biomarkers was most enhanced in patients with obstructive uropathies. A positive correlation between urinary TGF-beta1 and VEGF(165) excretion, shown both in patients and healthy controls, indicates an interdependent nature of their generation.     

Early tubular proteinuria and the development of nephritis in Henoch-Schönlein purpura

The prognosis of Henoch-Schonlein purpura (HSP) is mainly determined by the involvement of the kidney, but prognostic markers have not been established. To study the extent of tubular involvement in HSP and its relationship to the development of HSP nephritis, we measured the urinary excretion of two tubular marker proteins in 36 children with HSP. After admission, urinary N-acetyl-beta-D-glucosaminidase (NAG) was determined in 20 children and alpha1-microglobulin (alpha1-MG) in 16 children respectively. These values were compared with the biochemical data on admission, 1 month, 6 months, and 12 months later. A total of 198 24-h urine samples from healthy children were used for the establishment of reference data for NAG and alpha1-MG (mean+/-2 SD). Twenty-one patients had elevated excretion of either NAG (>mean+2 SD, n=12) or alpha1-MG (>mean+2 SD, n=9). The highest values (>mean+4 SD) were found in patients with early kidney involvement. Normal values were accompanied by a benign further clinical course. Children with intermediate high values (>mean+2 SD, 相似文献   

Urinary endothelin (ET1) in complete ureteric obstruction in the miniature pig

Summary Segmental renal scarring occurs in experimental obstructive uropathy in the multipapillary porcine kidney, and segmental abnormalities in renal perfusion are likely to be responsible. This preliminary study examines the urinary excretion of the potent locally active vasoconstrictor endothelin 1 (ET1) in a pig model of renal obstruction and subsequent relief. Significant urinary excretion of ET1 from the postobstructive kidney was found to occur after longstanding obstruction. Preglomerular arteriolar stenosis may be the cause of the renal ischaemia in ostruction that is at first reversible but later becomes irreversible if the stimulus persists. ET1 may be implicated in the pathogenesis of this injury.     

Effect of iron deficiency anemia on renal tubular function in childhood

Little is known about renal function in children with iron deficiency anemia. The purpose of this study was to investigate renal tubular function in these children. We compared renal tubular function in 20 children with iron deficiency anemia with 20 healthy age-matched controls. Blood and urine samples were obtained for hematological and biochemical analysis. Mean fractional excretion of sodium and mean urinary N-acetyl-beta- D-glucosaminidase/creatinine were significantly higher in the children with iron deficiency anemia than in controls (P<0.05). Hemoglobin levels were negatively correlated with urinary N-acetyl-beta- D-glucosaminidase/creatinine (r= -0.44, P=0.015), but were not correlated with fractional excretion of sodium (r= -0.29, P=0.13). There was no correlation between urinary N-acetyl-beta- D-glucosaminidase/creatinine and fractional excretion of sodium (r=0.32, P=0.09). The results suggest that children with iron deficiency anemia have impaired renal tubular function.     

Endogenous endothelins mediate increased acidification in remnant kidneys

Because endothelins (ET) mediate increased renal acidification induced by dietary acid and animals with reduced renal mass exhibit increased urinary ET-1 excretion, the hypothesis that ET mediate increased renal acidification in remnant kidneys was tested. Four weeks before the study, rats underwent a 5/6 nephrectomy (Nx) and a microdialysis apparatus was inserted into the remnant left kidney and the left kidney of sham-treated control animals, for measurements of renal ET-1 contents. Nx animals exhibited greater ET-1 addition to the renal dialysate than did control animals (681 +/- 91 versus 290 +/- 39 fmol/g kidney wt per min, P < 0.002) and greater urinary ET-1 excretion (346 +/- 79 versus 125 +/- 24 fmol/d, P < 0.02). Urinary net acid excretion rates were similar for Nx and control animals (732 +/- 106 versus 1005 +/- 293 microEq/d, P = 0.4), but Nx animals exhibited greater in situ HCO(3)(-) reabsorption in proximal (972.3 +/- 77 versus 482.6 +/- 42.4 pmol/min, P < 0.001) and distal (62.7 +/- 6.7 versus 24.3 +/- 2.5 pmol/min, P < 0.001) tubules. Orally administered bosentan, an ET(A/B) receptor antagonist, decreased urinary net acid excretion in Nx animals (to 394 +/- 99 microEq/d, P < 0.04 versus without bosentan); the decrease was mediated by decreased HCO(3)(-) reabsorption in both the proximal and distal tubules. Furthermore, bosentan decreased blood base excess in Nx animals (0.1 +/- 0.3 to -0.12 +/- 0.03 microM/ml blood, P < 0.002), consistent with acid retention. The data demonstrate that endogenous ET mediate increased urinary acid excretion in the remnant kidneys of Nx animals.     

Possible role of prostaglandins in pathogenesis of nocturnal enuresis in children

OBJECTIVE: To compare excretion of ions and prostaglandins by the kidney in children with noctural enuresis. MATERIAL AND METHODS: Thirty-two children with primary nocturnal enuresis and 23 normal children were examined. Osmolality and sodium and potassium concentrations were measured in their urine and blood serum. Prostaglandins E2, E1, and F2alpha were determined using kits for immunoenzyme analysis. Luminal and contraluminal prostaglandin secretions were studied in frog urinary bladder. RESULTS: Children with nocturnal enuresis have increased nocturnal diuresis and renal sodium excretion, but no increase was found in excretion of prostaglandins E2, E1, and F2alpha. Administration of sodium diclofenac before bed-time eliminated episodes of nocturnal enuresis in 37% of children; intranasal administration of Adiuretin SD had a positive effect in 69% of enuretics. In children with nocturnal enuresis there is a correlation between renal excretion of PGE2 and sodium ions; this correlation is absent in the control group children, and disappears in enuretics treated with desmopressin. To evaluate the representativeness of the data on prostaglandin secretions to urine as compared with their release to extracellular fluid, experiments on frog urinary bladder were performed: a correlation was found between prostaglandin secretion to the urinary bladder lumen and to the extracellular fluid. CONCLUSIONS: The results of the study suggest that changes in renal function are due not to a higher secretion of prostaglandins in nocturnal enuresis but to the relative dominance of their effect as compared with other physiologically active substances that simultaneously act on renal tubular cells.     

MCP-1 and EGF renal expression and urine excretion in human congenital obstructive nephropathy

BACKGROUND: Obstructive nephropathy is characterized at the histologic level by tubular atrophy and interstitial monocyte infiltration. The molecular mechanisms underlying these histologic changes are still poorly defined. Epidermal growth factor (EGF) produced by tubular cells seems to play a pivotal role in the modulation of tubular cell growth, while monocyte chemotactic peptide-1 (MCP-1) is a powerful and specific chemotactic and activating factor for monocytes. METHODS: Twenty-four patients with congenital ureteropelvic junction obstruction [UPJO; 10 with recurrent urinary tract infection (UTI) and 10 with no UTI] and 15 healthy children were studied. Diagnosis was made by renal ultrasound, intravenous pielography, and MAG3 scan. Urinary samples were collected before and after surgery. In 10 patients, urine was also collected directly from the affected pelvis at the time of surgery. Urinary EGF and MCP-1 levels were measured by enzyme-linked immunosorbent assay. MCP-1 and EGF gene expression were evaluated by in situ hybridization in 15 biopsies from congenital UPJO and in 10 normal kidneys. RESULTS: In normal kidneys, there was a high expression of EGF mRNA, whereas MCP-1 mRNA was undetectable. MCP-1 gene expression was strikingly increased at the tubulointerstitial level in UPJO biopsies compared with controls and was directly correlated with the extent of monocyte infiltration. In addition, UPJO kidney sections showed a marked reduction in EGF gene expression that was directly correlated with the degree of tubular damage. EGF urine concentration was significantly reduced in UPJO when compared with control and directly correlated with its renal gene expression. On the other hand, the MCP-1 urine concentration was strikingly increased in UPJO patients. It is noteworthy that a significant and inverse correlation was observed between the MCP-1 concentration in the urine collected from the obstructed pelvis and the MAG3 clearance of the obstructed kidney (r = -0.76). The presence of recurrent UTI was associated with a significantly higher MCP-1 excretion and a slight reduction in EGF urine concentration. The surgical correction of UPJO was followed by an improvement of renal function together with a significant reduction in MCP-1 excretion and a marked increase in EGF urine concentrations. Interestingly, EGF urine concentration measured before surgery was significantly correlated with the difference between the MAG3 clearance of the obstructed kidney before and after surgery. CONCLUSIONS: MCP-1 and EGF seem to be involved in the pathogenesis of tubulointerstitial damage in congenital obstructive nephropathy, and their urine excretion may represent a powerful prognostic marker in this form of renal disease.     

Involvement of renal nerves and endothelins in the regulation of renal water excretion in diabetes insipidus rats

The interaction between renal nerves, endothelins acting via endothelin-A receptors and vasopressin in the regulation of renal excretory function was investigated. In conscious intact and renal denervated diabetes insipidus (DI) Brattleboro rats, as well as their controls, Long-Evans (LE) rats, an infusion of 16.4 nmol/kg/min ET(A) receptor antagonist BQ-123 was performed in the course of 50 min. Femoral artery blood pressure, heart rate, Ccr, V x U(Na), V x U(K) and V x U(Cl) did not alter in any of the groups. Urine flow rate diminished by 38.1% (p < 0.02), while urine osmolality increased by 30.3% (p < 0.05) as a result of BQ-123 infusion in the intact LE rats but neither urine flow rate nor urine osmolality changed in the DI rats. In contrast to intact LE rats, BQ-123 infusion in renal denervated LE rats did not alter urine flow rate or urine osmolality. However, urine flow rate in renal denervated DI rats surprisingly decreased by 71.1% (p < 0.01) while urine osmolality increased by 161% (p < 0.001) as a result of BQ-123 infusion. Endogenous endothelins can regulate renal water excretion through ET(A) receptor activation. Renal sympathetic nerves participate in the modulation of renal water excretion influencing the ET(A) receptor-mediated effects of endothelins in the kidney.     

The Urinary Excretion of Deoxypyridinium Cross-Links is Higher in Diabetic Than in Nondiabetic Adolescents

We have measured the urinary excretion of deoxypyridinium (D-Pyr) crosslinks, a sensitive and specific marker of bone resorption, in morning urine in 102 healthy, nonhospitalized, Caucasian subjects (8–18 years) and in 18 diabetic subjects (12–17 years). The free D-Pyr crosslinks were measured using the Pyrilinks D-Assay. In the diabetic subjects, plasma glucose was regulated throughout the night by a constant infusion of insulin and a variable infusion of 24% glucose. In the nondiabetic subjects, the excretion of D-Pyr increased until 12–14 years of age, and thereafter decreased, and the excretion of D-Pyr/hour was correlated with the height Z-score. The excretion of D-Pyr/hour and the D-Pyr/creatinine ratio was higher in the diabetic adolescents than in the nondiabetic adolescents. In subjects over the age of 12, the D-pyr/creatinine ratio was higher in males than in females. In conclusion, in healthy children and adolescents, the excretion of D-Pyr peaks at 12–14 years of age. The D-Pyr excretion is higher in diabetic than in nondiabetic adolescents, suggesting increased bone resorption in diabetic adolescents. Received: 8 May 1997 / Accepted: 10 January 1999     

Increased urinary adrenomedullin excretion in children with urinary-tract infection

Background: Adrenomedullin (AM), a smooth-muscle relaxant peptide, is stimulated by cytokines and bacterial endotoxins. We hypothesized that urinary-tract infections may be associated with elevated urinary AM excretion. Methods: AM in urine was quantified in eleven children with urinary-tract infection and 11 age- and sex-matched controls by radioimmunoassay. RT-PCR was used to demonstrate local AM mRNA expression in the urinary tract. Results: In healthy controls but not in diseased children there was a significant correlation between AM and creatinine in urine (r-0.91, P<0.001). AM levels in children with urinary tract infection were significantly higher than in controls (0.6±0.41 vs 0.15±0.14 ng/&mgr;mol creatinine; P<0.001; (means±SD)). There was a significant correlation between white cell count and AM in urine (r-0.78, P<0.001). AM mRNA was expressed in renal tissue, renal pelvis, ureter, bladder, and urethra. Conclusion: The smooth-muscle relaxant peptide adrenomedullin that is synthesized in tissue of the human urinary tract is elevated in urine of patients with urinary-tract infections. A possible consequence might be the interference with the ureteral anti-reflux mechanisms.     

N-Acetyl-β-d-glucosaminidase excretion in healthy children and in pediatric patients with urolithiasis

Hyperoxaluria was reported to induce renal damage, probably due to toxic effects on renal tubules. Such tubular damage might be expressed by an increase in urinary excretion of marker enzymes such as N-acetyl-β-d-glucosaminidase (NAG). We set out to examine a possible relationship between the excretion of NAG and that of urinary lithogenic and stone-inhibitory substances by analyzing 24-h urine specimens from 56 children with urolithiasis and 25 healthy children with normal renal function and without a history of urolithiasis. The NAG excretion was higher in patients with urolithiasis (3.5 ± 0.51 U/g creatinine) as compared with healthy subjects (1.33 ± 0.14 U/g creatinine, P < 0.05). A positive correlation between NAG and oxalate excretion was observed in female patients (r = 0.56; P < 0.01). In conclusion, the increase in urinary NAG in children with urolithiasis might express renal tubular damage. It seemed, however, not to be specifically related to the excretion of a single lithogenic substance.     

Urinary epidermal growth factor in different renal conditions in children

Several studies have demonstrated the important role of growth factors, particularly epidermal growth factor (EGF) and transforming growth factor alpha (TGFalpha), in cellular growth after renal damage. EGF is mainly synthesized by the kidney. Many studies indicate that urinary EGF concentration significantly decreases in patients with acute and chronic renal failure. In this study we determined urinary EGF concentrations in children with renal and/or urological pathologies. We investigated 38 patients, 17 males and 21 females, of 3.34+/-2.96 years (mean +/- standard deviation), who were followed in the Nephrologic Unit of the Pediatric Department of the University of Verona for recurrent urinary tract infections: seven of these had vesicoureteric reflux and 4 had hypodysplasia. The results were compared with those from a healthy age-matched group of 44 children. In all patients, we assessed renal function including an examination of the urine with a microbiological evaluation. Moreover, a renal ultrasound and a voiding cystourethrogram were performed.     

Silicon metabolism. I. Some aspects of renal silicon handling in normal man

Renal silicon handling was investigated in 23 healthy adults using electrothermal atomic absorption techniques. The mean urinary silicon excretion was 33.1 +/- 3.85 mg/day; the mean renal silicon clearance was 88.6 +/- 7.94 ml/min; the mean fractional excretion of silicon was 86.35 +/- 8.1%, and the mean urine silicon concentration was 0.265 micrograms/ml. Using multiple correlation analysis, the urinary silicon was found to be highly significantly correlated with the urine magnesium concentration (p less than 0.001) and also with urinary sodium and urinary osmolality (p less than 0.01). 24-hour urinary silicon excretion was highly significantly correlated with fractional excretion of silicon (p less than 0.001), sodium (p less than 0.001), phosphorus (p less than 0.001), magnesium (p less than 0.001), and osmolar load. In split urine studies in 7 subjects urinary silicon was correlated highly significantly with urinary magnesium in all 7 and with urinary osmolality, urine calcium, and urine creatine concentration in 6 of 7. There was a highly significant correlation between renal silicon clearance and fractional excretion of silicon (p less than 0.0005), with magnesium excretion (p less than 0.01), and with sodium excretion. It is suggested that ion pairing of orthosilicate and magnesium may explain some of these urinary findings.     

Urinary excretion of podocytes in patients with diabetic nephropathy.

BACKGROUND: Detection of podocytes in the urinary sediments of children with glomerulonephritis has been shown to indicate severe injury to the podocytes. The aim of the present study was to determine whether podocytes are present in the urine sediments of adult patients with diabetes with and without nephropathy and whether trandolapril is effective for podocyte injury. METHODS: Fifty diabetic patients (10 with normoalbuminuria, 15 with microalbuminuria, 15 with macroalbuminuria and 10 with chronic renal failure) and 10 healthy controls were studied. Urinary podocytes were examined by immunofluorescence using monoclonal antibodies against podocalyxin, which is present on the surface of podocytes. In addition, we studied plasma metalloproteinase (MMP)-9 concentrations in all patients. RESULTS: Urinary podocytes were absent in healthy controls, diabetic patients with normoalbuminuria and diabetic patients with chronic renal failure. Podocytes were detected in the urine of eight diabetic patients with microalbuminuria (53%) and of 12 patients with macroalbuminuria (80%). The number of podocytes in the urine of patients with macroalbuminuria was significantly greater than in patients with microalbuminuria (P:<0.01). However, there was no relationship between urinary albumin excretion and urinary podocytes. In addition, plasma MMP-9 concentrations were significantly correlated with the number of urinary podocytes (P:<0.01). Twelve diabetic patients with macroalbuminuria and eight patients with microalbuminuria who had urinary podocytes were treated with the angiotensin-converting enzyme inhibitor trandolapril. Urinary albumin excretion, the number of podocytes and plasma MMP-9 concentrations were reduced by the trandolapril treatment. CONCLUSIONS: Podocytes in the urine may be a useful marker of disease activity in diabetic nephropathy. Trandolapril may be effective for podocyte injury.     

Detection of autosomal dominant polycystic kidney disease by NMR spectroscopic fingerprinting of urine

Autosomal dominant polycystic kidney disease (ADPKD) is a frequent cause of kidney failure; however, urinary biomarkers for the disease are lacking. In a step towards identifying such markers, we used multidimensional-multinuclear nuclear magnetic resonance (NMR) spectroscopy with support vector machine-based classification and analyzed urine specimens of 54 patients with ADPKD and slightly reduced estimated glomerular filtration rates. Within this cohort, 35 received medication for arterial hypertension and 19 did not. The results were compared with NMR profiles of 46 healthy volunteers, 10 ADPKD patients on hemodialysis with residual renal function, 16 kidney transplant patients, and 52 type 2 diabetic patients with chronic kidney disease. Based on the average of 51 out of 701 NMR features, we could reliably discriminate ADPKD patients with moderately advanced disease from ADPKD patients with end-stage renal disease, patients with chronic kidney disease of other etiologies, and healthy probands with an accuracy of >80%. Of the 35 patients with ADPKD receiving medication for hypertension, most showed increased excretion of proteins and also methanol. In contrast, elevated urinary methanol was not found in any of the control and other patient groups. Thus, we found that NMR fingerprinting of urine differentiates ADPKD from several other kidney diseases and individuals with normal kidney function. The diagnostic and prognostic potential of these profiles requires further evaluation.