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PubMed1990

Correlation of urinary albumin and beta-2-microglobulin and growth hormone excretion in patients with diabetes mellitus and short stature.

We examined the correlation between urinary GH, urinary albumin, and beta-2-microglobulin excretion to determine how the excretion of GH relates to markers of renal glomerular and tubular function. Urinary albumin and GH excretion was determined in timed daytime and nighttime urine collections obtained from both subjects with diabetes mellitus and subjects with short stature. For subjects with diabetes, urinary GH excretion rate correlated highly with urinary albumin concentration and excretion rate in both the range of 0 to 1.6 g/L (r = 0.75), P less than 0.001) and in the microalbuminuria range, 0 to 0.4 g/L (r = 0.53, P less than 0.001). Changes in GH and albumin excretion occurred in parallel in 71% of the subjects with diabetes and elevated albumin excretion. The mean GH excretion rate was higher in the group with elevated albumin excretion rate (AER) during both day and night compared to the group with microalbuminuria during the day and normal AER at night. For subjects with short stature, the mean albumin excretion rate was 0.7 +/- 1.3 micrograms/min (range 0.05-8.3 micrograms/min) using a sensitive enzyme-linked immunosorbent assay to measure albumin concentration. The correlation of GH and albumin excretion rates for the subjects with short stature was not statistically significant (r = 0.14, P less than 0.5). About half of the subjects with diabetes and elevated AER (greater than 10 micrograms/min) had a GH excretion rate within the range observed in subjects with short stature. The GH and albumin excretion rate were not correlated in this group. There was a positive correlation of both albumin and GH excretion rate with age in the subjects with diabetes. Urinary GH and beta-2-microglobulin excretion rates were determined in a larger group of subjects with diabetes and a separate group with short stature. Urinary GH and beta-2-microglobulin excretion were correlated both in subjects with diabetes (r = 0.46, P less than 0.001) and with short stature (r = 0.64, P less than 0.001). The association was present in urine collected either during the day or night. The mean GH excretion rate of the group with diabetes was greater than the group with short stature. In conclusion, there was an association of urinary GH and albumin excretion rate in subjects with abnormal glomerular function as indicated by elevated albumin excretion rate. An association of urinary GH and beta-2-microglobulin excretion was observed in subjects with normal tubular function.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1990

The renal excretion of selenium.

The excretion of selenium in urine was determined in West German healthy volunteers. Women excrete 17.7 +/- 4.2 micrograms Se/d and men 19.0 +/- 9.0 micrograms Se/d. The daily selenium excretion per gram creatinine is 13.5 +/- 3.8 micrograms Se/g crea for women and 9.8 +/- 3.3 micrograms Se/g crea for men. The clearance of selenium from the plasma is calculated with 0.18 mL/min. The selenium excretion per day is positively correlated with the 24 h excretion of urea and creatinine. The correlation of the selenium excretion with the urea excretion is most probably owing to the fact that the selenium intake of West Germans is linked primarily to foods with high protein contents. That the selenium excretion is directly correlated with the creatinine excretion is an indicator that the muscle, which accounts for nearly 50% of the whole body selenium in West German adults, influences the selenium excretion in urine. The positive correlation of the selenium excretion with the potassium excretion also indicates that the muscle mass contributes significantly to the selenium excretion in urine. Another indicator that the selenium excretion is influenced by the muscle is that after intensive muscular activity (running), selenium excretion is enhanced. The 24 h selenium excretion is dependent on the glomerular filtration rate of the kidney characterized by the creatinine clearance. This result is important, because if the selenium excretion is used as parameter for the selenium status of humans, the kidney function should be known. This is a limitation for the use of the urinary selenium excretion as parameter for the selenium status. This is especially important for patients whose glomerular filtration rate is low. The 24 h selenium excretion is further influenced by the 24 h urine volume. Selenium losses via urine may be concomitant with protein losses in urine.

Adult↗
PubMed2002

Urinary N-acetyl-beta-glucosaminidase excretion is a marker of tubular cell dysfunction and a predictor of outcome in primary glomerulonephritis.

BACKGROUND: The urinary excretion of N-acetyl-beta-glucosamynidase (NAG) is increased in subjects exposed to substances toxic for renal tubular cells. In experimental and human glomerular diseases, its increased excretion is probably due to the dysfunction of tubular epithelial cells induced by increased traffic of proteins in the tubular lumen. The first aim of this study was to evaluate whether NAG excretion is correlated not only with the amount of proteinuria but also with some proteinuric components which reflect both glomerular capillary wall damage (IgG) and an impairment of tubular reabsorption of microproteins (alpha(1) microglobulin). The second aim was to assess whether NAG excretion has a predictive value on functional outcome and response to therapy. METHODS: In 136 patients with primary glomerulonephritis [74 with idiopathic membranous nephropathy (IMN), 44 with primary focal segmental glomerulosclerosis (FSGS) and 18 with minimal change disease (MCD)] urinary NAG excretion was measured by a colorimetric method and expressed in units per gram of urinary creatinine. RESULTS: Using univariate linear regression analysis NAG excretion in all 136 patients was significantly dependent on IgG excretion, 24-h proteinuria, fractional excretion of alpha(1) microglobulin (FE alpha(1)m) and diagnosis. Using multiple linear regression analysis, NAG excretion was significantly dependent only on IgG excretion and 24-h proteinuria. Limiting the analysis to 67 patients with nephrotic syndrome (NS) and baseline normal renal function, by multiple linear regression, NAG excretion was significantly dependent on IgG excretion (P=0.0004), 24-h proteinuria (P=0.0067) and FE alpha(1)-m (P=0.0032) (R(2)=0.63). In 66 patients with NS and normal baseline renal function (MCD 10 patients; FSGS 20 patients; IMN 36 patients), according to values below or above defined cut-offs (IMN, </= or >18 U/g urinary Cr; FSGS and MCD, </= or >24 U/g urinary Cr), NAG excretion predicted remission in 86 vs 27% of IMN patients (P=0.0002) and 77 vs 14% of FSGS patients (P=0.005). Progression to chronic renal failure (CRF) was 0 vs 47% in IMN patients (P=0.001) and 8 vs 57% in FSGS patients (P=0.03). Using Cox model, in IMN patients only NAG excretion (P=0.01, RR 5.8), but not 24-h proteinuria, predicted progression to CRF. All MCD patients had NAG excretion values below the chosen cut-off, and 90% of them developed remission. Response to immunosuppressive therapy was significantly different in patients with NAG excretion values below or above the cut-offs. CONCLUSION: Urinary NAG excretion can be considered as a reliable marker of the tubulo-toxicity of proteinuria in the early stage of IMN, FSGS and MCD; the excretion values show a significant relationship with 24-h proteinuria, IgG excretion and FE alpha(1)m. Its determination may be a non-invasive, useful test for the early identification of patients who will subsequently develop CRF or clinical remission and responsiveness to therapy.

Acetylglucosaminidase↗
PubMed1991

Diurnal variation in urinary protein excretion in diabetic nephropathy.

We examined the diurnal variation in urinary excretion rate of albumin, IgG and beta 2-Microglobulin (beta 2-M) in healthy volunteers (n = 24), and in patients with type I diabetes mellitus having normal albumin excretion rate (less than 20 micrograms/min; n = 16), incipient diabetic nephropathy (albumin excretion rate 20-200 micrograms/min; n = 12) and clinical diabetic nephropathy (albumin excretion rate greater than 200 micrograms/min; n = 12). Diurnal variation was defined as [(overnight minus daytime): daytime excretion rate] times 100%. Median diurnal variation in albumin excretion rate in the various groups varied from -32 to -57%, and in IgG excretion rate from -42 to -65%, being not significantly different between the proteins or between the groups. Diurnal variation in beta 2-M excretion rate was similar in healthy volunteers and in patients with normal albumin excretion rate or incipient diabetic nephropathy (median -36 to -43%), but significantly reduced in patients with clinical diabetic nephropathy (median 0%; P less than 0.005), nine of whom had elevated beta 2-M excretion rates, suggesting tubular dysfunction. Except for beta 2-M excretion rate in patients with clinical diabetic nephropathy, the diurnal variations in albumin excretion rate, IgG excretion rate and beta 2-M excretion rate were larger than the diurnal variation in creatinine excretion rate (median -7 to -11%, P less than 0.005). Diurnal variations in albumin excretion rate and IgG excretion rate were highly correlated (r = 0.89, P less than 0.00001). These data suggest that similar mechanisms may account for diurnal variations in albumin excretion rate and IgG excretion rate.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1995

Urinary excretion of type IV collagen and laminin in the evaluation of nephropathy in NIDDM: comparison with urinary albumin and markers of tubular dysfunction and/or damage.

To clarify the diagnostic relevance of urinary type IV collagen (IV-C) and laminin in diabetic nephropathy, the excretion of these basement membrane proteins were determined by enzyme immunoassay in 172 non-insulin-dependent diabetic patients with different grades of nephropathy and 64 non-diabetic control subjects, and were evaluated in comparison with those of urinary albumin, N-acetyl-beta-D-glucosaminidase (NAG) and alpha 1-microglobulin (alpha 1MG). These excretions were also compared between a group of non-diabetic renal disease (NDRD) patients (n = 24) and a subgroup of the diabetic patients studied (n = 76), whose urinary albumin excretion (UAE) varied within the ranges of micro- and macroalbuminuria. Of the diabetic patients studied, 49.7%, 53.4% and 32.4% had raised urinary albumin, NAG and alpha 1 MG excretion, respectively. In these patients, 54% and 53% exceeded the upper limit of normal for urinary IV-C and laminin. The level of IV-C and laminin excretion and the prevalence of their abnormal excretion showed a trend to increase with increasing grade of nephropathy, as assessed by UAE. In the normoalbuminuric [UAE < 20 mg/g creatinine (Cr)] stage, 28.3% and 26.3% patients had raised urinary IV-C and laminin excretion, respectively. In this stage, the excretion values for IV-C and laminin also rose significantly even when the UAE was < or = 10 mg/g Cr (P < 0.05 and P < 0.005, respectively). There was a close linear relationship between IV-C and laminin excretion (r = 0.73, P < 0.0001), together with their significant relationships with albumin, NAG and alpha 1MG excretion. The relationship of urinary IV-C and laminin with urinary NAG and alpha 1MG excretion remained significant even in normoalbuminuric patients. The normoalbuminuric patients with raised NAG and/or alpha 1MG excretion also had a higher prevalence of raised IV-C and laminin excretion than those with normal NAG and alpha 1MG excretion. The excretion values for IV-C and laminin, and the excretion ratios for IV-C/albumin and laminin/albumin were significantly higher in diabetic patients with evidence of incipient and clinical nephropathy than in NDRD patients, though the two patient groups had a comparable level of serum Cr and UAE. We conclude that the measurement of urinary IV-C and laminin may have potential for the evaluation of diabetic nephropathy. Furthermore, their determination might be helpful for distinguishing diabetic versus non-diabetic etiologies of altered renal function in diabetic patients.

Acetylglucosaminidase↗
PubMed2000

Renal kallikrein excretion: role of ethnicity, gender, environment, and genetic risk of hypertension.

BACKGROUND AND OBJECTIVE: Alterations in renal kallikrein excretion are well-described in hypertension, and kallikrein excretion may predict risk of developing hypertension, but kallikrein excretion has not been directly compared across several ethnic strata, nor have the effects of ethnicity, gender, environment, and genetic risk of hypertension been simultaneously considered as determinants of kallikrein. METHODS: We investigated determinants of kallikrein excretion in a cross-section of n = 204 normotensive subjects stratified by ethnicity (119 Caucasian, 33 African-American, 52 Asian), gender (109 men, 95 women), environment (spontaneous electrolyte intake/excretion), and heredity (genetic risk (family history) of hypertension). Results were interpreted by analysis of variance (with Bonferroni post hoc comparison corrections), analysis of covariance, multiple linear regression, and maximum likelihood. RESULTS: Urinary kallikrein activity varied substantially (F = 5.30, P = 0.006) across the three ethnic groups, with African-American values approximately 50% lower than Caucasian (P = 0.005) or Asian (P = 0.02). Ethnicity and gender (T = 3.24, P = 0.001) had independent effects on kallikrein, with women excreting approximately 50% more kallikrein than men, regardless of ethnicity. Subjects at genetic risk of hypertension were over-represented (P = 0.048) in the lower stratum of a bimodal distribution of kallikrein excretion (chi-square = 29.6, P < 0.001). Potassium excretion was diminished in African-Americans (P < 0.001 to P = 0.002), and in a multivariate analysis, potassium excretion was the strongest correlate of kallikrein excretion (T = 4.10, P = 0.0001). In a subset of Caucasian and African-American individuals, African-Americans exhibited diminished excretion of not only kallikrein and potassium, but also aldosterone (P = 0.003), suggesting a mechanistic link between potassium and kallikrein excretion in their ethnic variations. CONCLUSIONS: Kallikrein excretion is influenced by several independent determinants, both hereditary (gender, ethnicity, and genetic risk of hypertension) and environmental (potassium intake and excretion). Ethnicity and environment may interact uniquely to influence kallikrein, as demonstrated by the case of African-Americans with diminutions of both kallikrein and potassium excretion. These results suggest a mechanism whereby kallikrein excretion is diminished in African-Americans, as well as therapeutic strategies to correct this deficiency. Finally, the identified determinants of kallikrein excretion will require analytic adjustment during genetic studies of this 'intermediate phenotype' in hypertension. Journal of Human Hypertension (2000) 14, 461-468

Adult↗
PubMed1995

Pulsatile urea excretion in the ureagenic toadfish Opsanus beta: an analysis of rates and routes

This study focused on the rates and routes of urea-N and ammonia-N excretion in the ureagenic toadfish and on the possibility that urea-N excretion occurs in pulses. Experimental approaches included the following: confinement in small individual containers with automated hourly sampling of water to follow temporal excretion patterns; divided chambers to separate excretion from the anterior and posterior parts of the fish; collection of urine and rectal fluid via chronic indwelling catheters; and gavage with [14C]-labelled polyethylene glycol 4000 to detect regurgitation of gastrointestinal fluids. When a standardized 'crowding' pre-treatment was employed to induce ureotelic behaviour, the fish exhibited significant elevations in the activity of glutamine synthetase in liver, kidney and gills, elevated plasma and bile urea-N levels, but unchanged ammonia-N and urea-N levels in most other body fluids. Unencumbered ureotelic fish confined in small containers excreted 82 % of their waste-N as urea-N and 18 % as ammonia-N; almost all (94 %) of this urea-N excretion occurred in a single pulse of less than 3 h duration about once every 24 h. This daily pulse did not occur by regurgitation of gut fluids, by excretion through prominent pores behind the pectoral fins or by discharge of rectal fluid or urine. Intestinal and urinary excretion accounted for less than 10 % of whole-body urea-N excretion and a negligible fraction of ammonia-N excretion. Pulsatile urea-N excretion occurred at the head end across the gills and/or body surface. Ammonia-N excretion, which was not pulsatile, also occurred largely through the head end. However, once the toadfish had been placed in divided chambers, urea-N excretion became continuous rather than pulsatile, and ammonia-N excretion increased greatly. A severe stress response was indicated by high levels of plasma cortisol, and the skin, which lacks scales, became a significant route of both ammonia-N and urea-N excretion. We speculate that the normal adaptive significance is that ureotelism facilitates cryptic behaviour, allowing the toadfish to virtually eliminate N-waste excretion during long periods while it remains sheltered in burrows. However, during severe stress, the effects of extremely high cortisol levels overwhelm the ammonia and urea retention mechanisms, and both substances leak across the general body surface.

Journal Article↗
PubMed2004

Supplementary concentrate type affects nitrogen excretion of grazing dairy cows.

These experiments were designed to investigate nutritional means of reducing urine N excretion by grazing cows. In experiment 1, 36 Holstein-Friesian cows averaging 92 d in milk were fed either 1 or 6 kg of a high protein concentrate or 6 kg of a low protein concentrate. Pasture dry matter (DM) intake was higher for cows fed 1 kg of high protein concentrate (15.4 +/- 0.62 kg/d) than for cows fed 6 kg of low protein concentrate (13.4 +/- 0.55) but not for cows fed 6 kg of high protein concentrate (13.9 +/- 0.96). The reduction in pasture intake per kg of concentrate DM ingested amounted to 0.35 and 0.47 kg of pasture DM for cows fed 6 kg of high protein and 6 kg of low protein concentrate, respectively. Milk yield and milk protein yield were higher for cows fed 6 kg of high protein concentrate than for cows fed 1 kg of high protein concentrate. Cows fed 6 kg of high protein concentrate had the highest levels of N intake, total N excretion, and urine N excretion. The proportion of N excreted in the urine was lowest for cows fed 6 kg of low protein concentrate. Milk N excretion as a proportion of ingested N was higher for cows fed 6 kg of low protein concentrate than for cows fed 6 kg of high protein concentrate but not for cows fed 1 kg of high protein concentrate. In experiment 2, 24 Holstein-Friesian cows averaging 211 d in milk were supplemented with 4 kg of rolled barley or 4.32 kg of NaOH-treated barley. Milk yield and milk protein yield tended to be higher for cows fed rolled barley than for cows fed NaOH-treated barley. There was no difference in N intake, fecal N excretion, urinary N excretion, or milk N output between diets. Milk urea N concentration was lower for cows fed rolled barley. Significant positive linear relationships were found between N intake and fecal N excretion, urine N excretion, and milk N excretion in experiment 1. In experiment 2, the relationships between N intake and fecal N excretion and urine N excretion were curvilinear, with urine N excretion increasing at a decreasing rate, and fecal N excretion increasing at an increasing rate, as N intake increased. The N excreted by dairy cows may be partitioned to fecal N if supplements based on high concentrations of fermentable organic matter and low concentrations of N are fed. Refinement of this nutritional strategy may allow reduced N excretion without reducing animal performance.

Animals↗
PubMed2002

Ethnic differences in titratable acid excretion and bone mineralization.

PURPOSE: To test our hypothesis that differences in urinary calcium excretion among blacks and whites may be secondary to ethnic variations in acid (H(+)) metabolism and to prove that increases in titratable acid excretion would be found among individuals predisposed to the development of stress fractures. METHODS: We administered 8 g NH(4)Cl acutely to 11 black and 18 white healthy volunteers and measured urinary sodium, calcium, and acid excretions. We measured the Na(+)/H(+) antiporter activity using acid-loaded platelets as surrogate markers for this exchanger expressed in renal epithelial cells. We also compared differences in titratable acid excretion among a cohort of subjects with, and without, a history of stress fracture. RESULTS: NH(4)Cl-induced increases in titratable urinary acid correlated with changes in the renal excretion of calcium and sodium, and stimulated acid excretion correlated with basal acid loss. Despite comparable changes in plasma pH, whites, when compared to blacks, had much greater basal acid excretion and NH(4)Cl-induced acid excretion. Whites also had much greater baseline calcium excretion rates when compared to blacks. Following acid loading, whites continued to exhibit greater calcium excretion rates than blacks. Acid loading significantly decreased sodium excretion in whites but not in blacks. Blacks also had significantly attenuated Na(+)/H(+) exchange activity. In a cohort of resting, athletic students, we found enhanced basal H(+) and phosphate excretion among subjects who experienced stress fractures during their rigorous physical training when compared to those individuals who did not. CONCLUSION: Blacks may have a greater endogenous buffering capacity than whites, or the reported ethnic differences in sodium and calcium excretion rates between blacks and whites may be secondary to racial variations in renal H(+) excretion. We conclude that both ethnic differences in bone mineralization and bone integrity in athletes are mediated by heritable differences in titratable acid excretion.

Acid-Base Equilibrium↗
PubMed1976

The effect of the anions, phosphate and sulphate, on normal rates of excretion of potassium in dogs.

Small doses of (NH4)2HPO4 or KH2PO4 by stomach tube caused increase in plasma PO4 and PO4 excretion. Above a threshold of 0-8 mmol. 1(-1), increase of plasma PO4 by 0-5 mmol. 1(-1) caused PO4 excretion to increase by about 35 mumol. min.-1 After KH2PO4 this relationship was not altered by the concurrent increases in plasma K and K excretion. After doses of (NH4)2SO4 or K2SO4, excretion of SO4 was similarly related to plasma SO4 and was independent of plasma K and K excretion. An effect of PO4 on K excretion was observed after doses of (NH4)2HPO4, when increased excretion of PO4 was accompanied by increased excretion of K without change in plasma K. There was also increased excretion of NH4 and a small increase in Na excretion. The changes were similar to those produced by (NH4)2SO4 [O'Connor and Summerill, 1976]. KH2PO4 and K2SO4 produced increase in plasma K and increased excretion of K not significantly different from the changes produced by KCl or KHCO3 [Baylis and O'Connor, 1976]. After KH2PO2 or K2SO4, the urinary anion was PO4 or SO4, instead of Cl and HCO3. Any effect of anions on K excretion was much less than the effect of increase in plasma K. At low rates of excretion of K, increased urinary excretion of impermeant anion can determine increased excretion of K. However, the effect of anion is small in comparison with the effect of increase in plasma K.

Animals↗
PubMed1996

Changes in the urinary excretion of creatinine, albumin and N-acetyl-beta-D-glucosaminidase with increasing age and maturity in healthy schoolchildren.

UNLABELLED: Raised urinary levels of albumin and N-acetyl-beta-D-glucosaminidase (NAG) are predictive of abnormal renal function and excretion of these substances is often expressed as a creatinine ratio. However, it is important to establish normal reference limits of albumin and NAG excretion for comparison of values from patients. For this reason, overnight excretion rates of creatinine, albumin and NAG were determined in timed overnight urine samples from 528 healthy schoolchildren (260 boys, 268 girls; 4-16 years) of normal size. There was a significant correlation with age and puberty for all substances in both sexes (P < 0.01). Peak creatinine excretion occurred at 16 years in boys, at 15 years in girls and at pubertal stage 5 in both sexes. Maximum albumin excretion was seen at 15 years and genital stage 5 in boys and at 16 years and breast stage 4 in girls. Peak NAG excretion occurred earlier, at 14 years and genital stage 4 in boys and at 13 years and breast stage 3 in girls. Boys excreted significantly more creatinine compared with girls before and during puberty (reflecting greater muscle mass) (P < 0.001) while excretion rates for albumin and NAG were similar in both sexes. Height and weight combined accounted for 58% and 29% of the variation in creatinine and NAG excretion respectively, while height alone predicted 20% of variation in albumin excretion. CONCLUSION: Age and puberty influence the urinary excretion of albumin and NAG while sex has an additional effect on creatinine excretion. The urinary excretion of albumin and NAG in children with renal disorders should be compared with age-related normal ranges while creatinine excretion could be used as a marker of muscle growth.

Acetylglucosaminidase↗
PubMed2001

Urinary excretion of IgG and alpha(1)-microglobulin predicts clinical course better than extent of proteinuria in membranous nephropathy.

In idiopathic membranous nephropathy (MN), the main predictors for progression to chronic renal failure (CRF) are the amount of proteinuria and extent of tubulointerstitial damage. The aim of this study is to evaluate whether urinary excretion of proteins reflecting the alteration of permselectivity in the glomerular capillary wall, such as immunoglobulin G (IgG), and the reabsorption impairment of low-molecular-weight proteins, such as alpha(1)-microglobulin (alpha(1)m), correlates with the extent of tubulointerstitial damage and have a predictive value for functional outcome and response to therapy better than 24-hour proteinuria. In 78 patients with MN, urinary excretion of albumin, transferrin, IgG, and alpha(1)m was measured by immunonephelometry in second-morning urine samples and expressed in milligrams per gram of urinary creatinine (uCr). In 48 patients with characterization of proteinuria and renal biopsy performed at the same time, excretion of IgG (P = 0.0087) and alpha(1)m (P = 0.0024), but not albumin (P = 0.37), transferrin (P = 0.38), or 24-hour proteinuria (P = 0.32), was associated significantly with the extent of tubulointerstitial damage (score, 0 to 1 versus >/=2). Only alpha(1)m excretion was associated significantly with global glomerular sclerosis (P = 0.0032) and arteriolar hyalinosis (P = 0.0004). Moreover, urinary excretion of alpha(1)m was significantly dependent on IgG excretion (r = 0.67; P = 0.0001), but not on albumin (P = 0.66) or 24-hour proteinuria (P = 0.07). Functional outcome could be evaluated in 38 patients with nephrotic syndrome and baseline normal renal function (serum creatinine, 0.99 +/- 0.20 mg/dL; follow-up, 44 +/- 22 months). Remission was 100% versus 20% in patients with IgG excretion less than 110 mg/g uCr versus 110 mg/g uCr or greater (P = 0.0001) and 77% versus 17% in patients with alpha(1)m excretion less than 33.5 mg/g uCr versus 33.5 mg/g uCr or greater (P = 0.0009), respectively. In patients with IgG and alpha(1)m excretion less than or greater than the cutoff value, progression to CRF was 0% versus 35% (P = 0.0026) and 0% versus 58% (P = 0.0001), respectively. Nineteen patients treated with immunosuppressive therapy were compared with 19 untreated patients. There was no difference in remission or progression between treated and untreated patients when IgG and alpha(1)m excretion were less than the cutoff value. There was a significant difference for progression to CRF between treated and untreated patients when alpha(1)m excretion was greater than the cutoff value (17% versus 100%; P = 0.0076). In conclusion, IgG excretion is associated significantly with the extent of tubulointerstitial damage and alpha(1)m excretion. This observation supports the hypothesis that IgG may be the toxic moiety of proteinuria. Excretion of IgG and alpha(1)m has a significant predictive value for both remission and progression and is useful to identify patients who are at risk for progression and for whom treatment with immunosuppressive therapy is indicated soon after diagnosis.

Albuminuria↗
PubMed2000

Long-acting natriuretic peptide, vessel dilator, and kaliuretic peptide enhance the urinary excretion rate of beta2-microglobulin.

The atrial natriuretic peptide (ANP) gene synthesizes a 126-amino acid (aa) prohormone from which four peptide hormones are derived. These 4 peptide hormones consisting of aa 1 to 30 (ie, long-acting natriuretic peptide [LANP]), aa 31 to 67 (vessel dilator), aa 79 to 98 (kaliuretic peptide), and aa 99 to 126 (ie, ANP) have diuretic, natriuretic, and/or kaliuretic properties. ANP has been reported to have its natriuretic and protein-excreting effects via both the proximal and distal tubules, but where in the kidney the other three peptide hormones have their natriuretic and/or diuretic effects is unknown. Further, it has never been investigated as to whether these three other peptide hormones enhance protein excretion. The present investigation was designed to determine (1) if these atrial peptides enhance protein excretion and (2) if their effects involve the proximal tubules of healthy humans by examining the excretion rate of beta2-microglobulin, a marker of proximal tubule function. Twenty-four healthy human subjects were studied following the infusion of 100 ng/kg body weight/min for 60 minutes of each of the respective peptides. LANP enhanced the excretion rate of beta2-microglobulin 2-fold within 20 minutes of beginning its infusion (P < .05) and was 2.5-fold higher than the preinfusion excretion rate at the end of the infusion. The excretion rate of beta2-microglobulin continued to be significantly (P < .01) increased for 3 hours after cessation of the LANP infusion, with the maximal excretion rate (ie, 3.8-fold increase) at 2.5 hours after stopping the infusion. Vessel dilator showed a more marked enhancement of beta2-microglobulin during its infusion, with the excretion rate increasing 2.5-fold at 20 minutes, and was increased 4-fold (P < .01) at the end of the infusion. With cessation of the vessel dilator infusion, the excretion rate of beta2-microglobulin decreased but was still elevated 2-fold (P < .05) 3 hours after stopping the infusion. Kaliuretic peptide enhanced the beta2-microglobulin excretion rate a maximal 3-fold, which occurred at the end of its infusion. The beta2-microglobulin excretion secondary to kaliuretic peptide remained 2-fold (P < .05) above baseline during the 3-hour postinfusion period. These peptide hormones similarly enhanced the albumin and total protein excretion rates 2- to 4-fold. These results indicate that LANP, vessel dilator, and kaliuretic peptide each (1) enhance protein excretion in healthy humans and (2) inhibit proximal tubular protein reabsorption.

Adult↗