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PubMed1967

Biliary excretion of foreign compounds. Biphenyl, stilboestrol and phenolphthalein in the rat: molecular weight, polarity and metabolism as factors in biliary excretion.

1. The extent of biliary excretion of biphenyl, tetralin, stilboestrol and phenolphthalein was studied in the rat. 2. Biphenyl and its 4-hydroxy and 4,4'-dihydroxy derivatives are extensively excreted in the bile as glucuronides in amounts increasing in order of molecular weight. 3. Stilboestrol and its glucuronide are excreted almost quantitatively in the bile mainly as the monoglucuronide, as are also phenolphthalein and its glucuronide. 4. Tetralin is excreted to the extent of about 13% of the dose, mainly as ac-tetralyl glucuronides. 5. The results and those of Abou-El-Makarem, Millburn, Smith & Williams (1967) are discussed and it is concluded that the extent of biliary excretion of foreign compounds in rats depends on their molecular weight and their possessing a strongly polar anionic group. There appears to be a minimum value of this molecular weight below which little biliary excretion (i.e. not more than 5-10% of the dose) occurs. There is some latitude in the choice of this molecular weight, which is about 325+/-50. The necessary molecular weight and polar group can be acquired by metabolism. Above this minimum value biliary excretion increases with molecular weight. It is suggested that the mechanism of the biliary excretion of foreign compounds may be similar to that of conjugated bile acids, which are highly polar and whose molecular weights exceed 400.

Journal Article↗
PubMedDate not supplied

[Blood urea concentration, a parameter for the assessment of protein metabolism in pregnant sows. 2. Relations between blood urea concentration and urine nitrogen excretion as well as estimation of urine nitrogen excretion from the blood urea concentration].

The influence of supplementing the ration with the limiting amino acid lysine on N-excretion in urine and the urea concentration in the blood (UCB) is investigated in an experiment with pregnant young sows. In contrast or the basic ration the most satisfactory N-utilisation reflects itself after a lysine intake of 8.2 g/animal and day during the early phase of gestation and 8.6 g during the last phase of gestation both in a diminished N-excretion in urine and a lower UCB. The following correlation coefficients were calculated for the relation between UCB an N-excretion in urine: early phase of gestation: 0.177 (n = 37); last phase of gestation. 0.431 (n = 30); gestation as a whole: 0.416 (n = 67). In a second experiment methionine supplementation in the feeding of a ration with a deficit of sulphur-containing amino acids led to a significant decrease of N-excretion in urine (alpha = 5%). While UCB also significantly decreased 5 hours after feeding, UCB virtually did not react to a changed level of amino acid intake when the blood sample was taken before feeding. In a third experiment, in which 49 g N/animal and day were taken in, differences regarding N-excretion in urine and UCB between pregnant and non-pregnant animals could not be established. When the results published in the first communication (Herrmann and Schneider, 1981) are included, the following correlation coefficients for the relation between N-excretion in urine and UCB are the result: 0.716 (n = 182) for sampling before feeding and 0.808 (n = 133) for sampling 5 hours after feeding. The confidence range of the estimated function y = -2.97 + 1.233 chi for the relation between N-excretion in urine (y; g/animal and day) and UCB 5 hours after feeding (chi; mg/100 ml serum) as well as the variability values do not make it possible to estimate N-excretion in urine from UCB with satisfactory accuracy.

Animals↗
PubMed1996

Sodium excretion in relation to calcium and hydroxyproline excretion in a healthy Japanese population.

To evaluate whether habitual excess sodium intake is a significant risk factor for calcium loss, we studied the relation between calcium excretion and sodium excretion in 410 male and 476 female Japanese aged 20-79 y. They were apparently healthy, free-living, and consuming diets of their own choosing. We divided the subjects into two groups: 20-49 y olds and 50-79 y olds. In each group, we observed significant positive correlation between daily calcium excretion and daily sodium excretion in both sexes. Multivariate analyses revealed that in each age group the relation was still significant after sex, age, body weight, and protein, calcium, and phosphorus intakes were adjusted for. The increases in urinary calcium excretion were estimated to be approximately 0.6 and 1.0 mmol for a 100-mmol increment in urinary sodium excretion for the 20-49 y olds and 50-79-y olds, respectively. We also observed significant positive correlations between daily hydroxyproline excretion and daily sodium excretion in both sexes for both age groups. The relation was still significant after sex, age, body weight, and protein intake from meat and fish were adjusted for. The results suggest that individuals with high sodium intake may lose more calcium in their urine than those with low sodium intake.

Adult↗
PubMed1981

Effects of hydroflumethiazide in congestive heart failure: renal electrolyte excretion related to urinary thiazide excretion and aldosterone.

The effect of hydroflumethiazide (HFT) on renal excretion of sodium, chloride, and potassium was studied in congestive heart failure and related to urinary excretion of thiazide and aldosterone. HFT 75 or 150 mg was administered orally once daily for 4 days to 8 male patients with roentgenological evidence of enlarged heart and slight or no peripheral oedema receiving digitalis and controlled diet. Urinary excretion of HFT did not change after repeated doses, whereas urinary excretion of a metabolite increased significantly. Initially, HFT induced a significant increase in the urinary excretion of sodium and potassium. After repeated doses, the natriuretic effect declined gradually in 6 of the patients. There was consistently a small natriuretic effect and a large kaliuretic effect at high serum aldosterone concentrations and high urine aldosterone excretion rates, whereas at low aldosterone levels, there was a wide range in magnitude of these effects. Relationships of the log urinary excretion rate of HFT to the increase in urinary excretion rate of sodium, chloride, and potassium showed positive and significant correlations. It was concluded that reduced natriuretic effect of HFT in congestive heart failure is not due to reduced delivery of thiazide to renal tubular cells but to compensatory adjustments of the kidney in part induced by aldosterone.

Aged↗
PubMed1981

On the relationship between urinary PGE2 and PGF2 alpha excretion rates and urine flow, osmolar excretion rate and urinary osmolality in anesthetized rats.

A strong inverse relationship was found between the excretion rates of the prostaglandins PGE2 and PGF2 alpha and urine flow (and osmolar excretion rate) over a range of urine flow rates from 1.5 to 40 microliters . min-1 . g kidney weight-1, covering spontaneous variations and isotonic saline diuresis. These results suggest the operation of a negative feedback mechanism by which the diuretic action of the prostaglandins, as part of a defence system, counteracts excessive oliguria. PGE2 excretion did not correlate with either urinary kallikrein excretion or plasma renin concentration. When the concentrating mechanism was interfered with by reducing renal perfusion pressure to, or below 65 mmHg, and vasopressin was given i.v. PGE2 excretion rate roughly parallelled urine--and probably medullary interstitial osmolar activity. However, in hydropenic rats there was no correlation between urine osmolality (Uosm) and PGE2 excretion over a range of osmolalities from 500 to 2 500 mOsm . kg-1, nor any relationship between delta Uosm and delta PGE2 excretion. Thus, a high interstitial osmolar activity appears to be a prerequisite for the activation of PG-synthesis in the renal medulla, but another (other) yet undefined factor(s) play the major role as (a) determinant(s) for PG-excretion in vivo.

Animals↗
PubMed2000

Increased excretions of beta2-microglobulin, IL-6, and IL-8 and decreased excretion of Tamm-Horsfall glycoprotein in urine of patients with active lupus nephritis.

Tubulointerstitial nephritis is a less frequently recognized but important complication of systemic lupus erythematosus. We have investigated the cytokine beta2-microglobulin (beta2M) and Tamm-Horsfall glycoprotein (THG) excretions in the urine of systemic lupus erythematosus patients to identify indices for evaluation of tubulointerstitial inflammation in lupus nephritis (LN). Daily urine was collected from 15 patients with active LN, from 12 patients with inactive LN, and from 17 normal subjects. The amounts of soluble interleukin (IL) 2 receptor, IL-6, IL-8, beta2M, and THG in urine were measured. Beta2M and THG were regarded as indicators of proximal and distal renal tubule function, respectively. The urinary excretions of IL-6 and IL-8 were significantly higher in patients with active LN than in those with inactive LN and in normal individuals. The excretion of soluble IL-2 receptor in all three groups of subjects was not significantly different. On the other hand, the excretion of beta2M in patients with LN was significantly higher than that in normal individuals. The excretion of beta2M in patients with active or inactive LN was not significantly different. The THG excretion was lower in patients with active LN and tubulointerstitial inflammation as compared with patients with inactive LN or normal individuals. Six patients underwent pulse cyclophosphamide therapy during the course of experiments. Five of them showed a decrease in IL-8 and IL-6 excretions in urine after the treatment. The excretions of beta2M and THG in urine, in addition to IL-6 and IL-8, can reflect the renal inflammatory activity in patients with lupus tubulointerstitial nephritis as well as in those having lupus glomerulonephritis.

Case-Control Studies↗
PubMed1988

Relation between renal and hepatic excretion of drugs. XI. Excretion of sulfonamides with various physico-chemical properties of different ages--influence of nephrectomy or bile duct ligation.

The pharmacokinetics of a series of 6-sulfonamides, with gradually increasing molecular weights, were studied in anaesthetized rats after intravenous bolus injection. Immature (20-day-old) and adult (55-day-old) rats were compared. In both age groups renal excretion of all sulfonamides tested here dominates (about 5- to 10-fold). In 20-day-old rats renal and hepatic excretions are immature and reach about 50% (liver) or 30% (kidney) of adult values. Relation between renal and hepatic excretion of sulfonamides is strongly correlated to the lipophilicity of these substances. Hepatic excretion of sulfonamides seems to be correlated to their pKa-values. Concerning their excretion via urine it is necessary to correlate different steps of renal transport to physico-chemical properties in detail. A general correlation between renal excretion of sulfonamides and their chemical structure obviously does not exist. After bile duct ligation 24 h before clearance experiments no compensatory increase of renal sulfonamide excretion occurs. 24 h following bilateral nephrectomy hepatic excretion of sulfonamides is significantly enhanced; however, this phenomenon is related to physico-chemical properties of the sulfonamides. Age differences in compensation of one elimination pathway do not exist.

Aging↗
PubMed1991

Biliary excretion of hexachloro-1,3-butadiene and its relevance to tissue uptake and renal excretion in male rats.

Renal, biliary, pulmonary and faecal excretion experiments were carried out with labelled hexachloro-1,3-butadiene [( 14C]HCBD) in male Sprague-Dawley rats, given orally (p.o.) and intravenously (i.v.) in doses of 1 and 100 mg kg-1 as a solution in polyethylene glycol. The radioactivity excreted over 72 h was determined in rats fitted with exteriorized biliary cannulae and in rats whose bile ducts remained fully functional, respectively. In addition, bile duct-duodenum cannula-linked rats, of which the donor was given 100 mg kg-1 [14C]HCBD orally and the recipient had also a bile fistula, were examined within 30 h for radioactivity in the excreta, the kidney, the liver and the plasma. In non-cannulated rats, fractional urinary excretion decreased when the dosage increased and amounted to 23% and 8.6% after i.v. injection or 18.5% and 8.9% after p.o. administration of 1 and 100 mg kg-1, respectively. Pulmonary excretion of radioactivity was less than 9% and was not affected by the increase in dosage. In bile duct-cannulated rats, fractional urinary excretions were similar irrespective of the dose and the route of administration and amounted to ca. 7.5% of the dose. Decrease in fractional biliary excretion occurred with increase in dosage (88.7% vs 72%) after i.v. injection and (66.8% vs 58%) after gavage. In cannulated rats, faecal excretion was less than 0.5% after i.v. injection and accounted for 3% and 16% of the dose after p.o. administration of 1 and 100 mg kg-1, respectively.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1975

Influence of volume expansion, serum sodium, and fractional excretion of sodium on urate excretion.

The relative contributions of volume expansion and increased fractional excretion of sodium to the uricosuria of saline infusion were assessed in 19 subjects by volume expansion with rapid infusion of 21 of hypertonic saline (3%), isotonic saline (0.9%), or hypotonic saline (0.45%). Urate excretion increased 385 mug/min (P less than 0.01) with hypertonic, 145 mug/min (P less than 0.05) with isotonic saline, and 294 mug/min (P less than 0.001) with hyptonic saline. When 150 meq of sodium chloride was administered as appropriate volumes of hypertonic, isotonic of hypotonic saline, the magnitude or uricosuria was correlated with volume load (r = 0.66, P less than 0.002). fractional excretion of sodium correlated with infusion volumes for all studies taken together (r = 0.35, P greater than 0.1). The relationship between fractional excretion of sodium and fractional excretion of urate was entirely attributed to their correlation with infusion volume. Both post-pyrazinamide urate excretion and pyrazinamide suppressible urate excretion increased with volume expansion.

Adolescent↗
PubMed1988

Relation between renal and hepatic excretion of drugs: VII. Hepatic and renal excretion of phenol red in thioacetamide-induced acute and chronic liver damage.

Acute and chronic liver damage was induced in rats by thioacetamide (TAA). Centrilobular liver cell damage associated with an accumulation of lipid droplets was produced by a single high dose (10 mg TAA/100 g b.m.). Liver fibrosis, micronodular and macronodular liver cirrhosis were induced by chronic TAA treatment (300 ml/l drinking water for 1.5, 3 or 6 months). Acute administration of TAA caused a significant decrease of hepatic phenol red excretion but no compensatory increase of its urinary excretion. In contrast, 24 h after bile duct ligation renal excretion of the dye increased by about 50%. After chronic exposure to TAA for three months hepatic phenol red excretion remained reduced and renal excretion raised significantly. This compensatory increase of urinary excreted phenol red amounts did not occur after 6 months of TAA treatment, probably as a result of additional nephrotoxicity of TAA. Two weeks after cessation of TAA exposure for 3 months, hepatic and renal phenol red excretion returned to normal. Bile flow per animal increased significantly after 3 months of TAA exposure. Apparently this is due to a reduced intrahepatic reabsorption of canalicular bile in TAA-damaged liver.

Animals↗
PubMed1988

Urinary excretion and diuretic action of furosemide in rats: increased response to the urinary excretion rate of furosemide in rats with acute renal failure.

A urinary excretion-response curve representing the urinary excretion rate of furosemide versus the urinary excretion rate of (Na+ + K+) was used to analyze furosemide action in rats with uranyl nitrate-induced acute renal failure (ARF) with and without dopamine coadministration. Urinary excretion of furosemide, but not its serum concentration, was the determinant for the diuretic action of furosemide. Increased diuretic response was observed in ARF rats, although the total diuretic response and urinary recovery of furosemide within 2 hr decreased. Dopamine enhanced furosemide-induced diuresis in ARF rats in terms of the total urine output and urinary electrolyte excretion, although the urinary excretion-response curves were not different. This enhancement by dopamine was found to be caused by the augmented urinary excretion of furosemide and the increased response to this drug in ARF rats. These findings suggest the contribution of decreased concentrating ability along the nephron and/or increased sensitivity of cells at the site of action to this drug.

Acute Kidney Injury↗
PubMed1997

Inulin and oligofructose do not influence the absorption of cholesterol, or the excretion of cholesterol, Ca, Mg, Zn, Fe, or bile acids but increases energy excretion in ileostomy subjects.

OBJECTIVE: To investigate the effects of inulin and oligofructose on cholesterol absorption and excretion of cholesterol, bile acids, energy, nitrogen and minerals in man. DESIGN: Double-blind cross-over study. SETTING: Metabolic kitchen with policlinic visits, Sahlgrenska Hospital, Göteborg, Sweden. SUBJECTS: Patients with conventional ileostomy because of ulcerative colitis. INTERVENTIONS: 7 g of inulin, 17 g of oligofructose and 7 g of sucrose were added to a controlled diet during three experimental periods of three days each. Ileostomy effluents were collected and analysed. Differences between experimental and control diet were investigated with the Wilcoxon's sign and values test. RESULTS: Inulin and oligofructose were recovered in the ileostomy effluent to 88% (95% CI, 76-100%) and 89% (64-114%) respectively. Dry solid excretion increased by 14.4 g (11.3-17.5) on inulin, and by 14.7 g (13.0-16.4 g) on oligofructose and energy excretion increased 245 kJ (190-307 kJ) on inulin and 230 kJ (214-315 kJ) on oligofructose compared to control diet (P < 0.05). Cholesterol absorption, excretion of cholesterol, bile acids, nitrogen, fat, calcium, magnesium, zinc and iron were not affected by inulin and oligofructose. CONCLUSIONS: Inulin and oligofructose are not digested in the small intestine. They do not affect mineral excretion and hence hardly mineral absorption. They do not increase fat or nitrogen excretion from the small intestine. Any physiological effect of inulin and oligofructose is probably mediated through other mechanisms than altered excretion from the small intestine.

Adult↗
PubMed2006

Ammonia excretion increased and urea excretion decreased in urine of a new world nectarivorous bat with decreased nitrogen intake.

We determined the effect of water and nitrogen intake on nitrogenous waste composition in the nectarivorous Pallas's long-tongued bat Glossophaga soricina (Phyllostomidae) to test the hypothesis that bats reduce excretion of urea nitrogen and increase the excretion of ammonia nitrogen as nitrogen intake decreases and water intake decreases. Because changes in urine nitrogen composition are expected only in animals whose natural diets are low in nitrogen and high in water content, we also measured maintenance nitrogen requirements (MNR). We hypothesized that, similar to other plant-eating vertebrates, nectarivorous bats have low MNR. Our nitrogen excretion hypothesis was partly proved correct. There was an increase in the proportion of N excreted as ammonia and a decrease in the proportion excreted as urea in low-nitrogen diets. The proportion of N excreted as ammonia and urea was independent of water intake. Most individuals were ureotelic (n = 28), and only a few were ureo-ammonotelic (n = 3) or ammonotelic (n = 2). According to our nitrogen requirement hypothesis, apparent MNR (60 mg kg(-0.75) d(-1)) and truly digestible MNR (54 mg N kg(-0.75) d(-1)) were low. A decrease in urea excretion in low-nitrogen diets may result from urea recycling from liver to the gut functioning as a nitrogen salvage system in nectarivorous bats. This mechanism probably contributes to the low MNR found in Pallas's long-tongued bats.

Ammonia↗
PubMed1995

Oat beta-glucan increases bile acid excretion and a fiber-rich barley fraction increases cholesterol excretion in ileostomy subjects.

The purpose of this study was to investigate whether oat beta-glucan is responsible for the increased bile acid excretion previously observed with oat-fiber diets. The excretion patterns in ileostomy subjects given diets containing oat-bran bread with and without added beta-glucanase, a beta-glucan-degrading enzyme, were compared. The effect of a beta-glucan-rich barley fraction on sterol excretion was also investigated. Nine ileostomy subjects were served four diets in random order, each diet for 2 consecutive days. Four different kinds of bread, mainly made from oat bran (OB diet, 12.5 g beta-glucan/d), oat bran with beta-glucanase (OBE diet, 3.8 g beta-glucan/d), barley (B diet, 13.0 g beta-glucan/d), or wheat flour (W diet, 1.2 g beta-glucan/d) were added to a basal diet. The 24-h excretion of bile acids was 53% higher in the OB diet period than in the OBE diet period (P < 0.05) and also was significantly higher than in the B and W diet periods (P < 0.05). Median (range) bile acid excretion was 851 (232-1550), 463 (123-1414), 755 (133-1187), and 606 (101-980) mg/d in the OB, OBE, B, and W diet periods, respectively. The excretion of cholesterol was significantly higher in the B diet period than in the OBE and W diet periods (P < 0.05), but the mechanism behind this effect of barley fiber is unknown. In oat bran, however, beta-glucan mediates an increase in bile acid excretion, which most probably explains the effect of oat fiber in lowering serum lipids.

Adult↗
PubMed1986

D-glucaric acid excretion in critical care patients--comparison with 6 beta-hydroxycortisol excretion and serum gamma-glutamyltranspeptidase activity and relation to multiple drug therapy.

The incidence of increased drug metabolism activity as a consequence of multiple drug therapy at a surgical intensive care ward has been studied non-invasively by determinations of daily urinary D-glucaric acid (GA) excretion rates. Among 165 randomly selected patients, GA excretion was stimulated in 76 cases (= 46%). Exploratory data analysis showed that increases in GA excretion are primarily due to administration of barbiturates (pentobarbitone, Nembutal), miconazole (Daktar) and, to a lesser extent, neuroleptics. Surprisingly, the large number of simultaneously administered additional drugs failed to increase GA excretion. Urinary 6 beta-hydroxycortisol (6 beta-OHF) and 17-hydroxycorticosteroid (17-OHCS) excretion rates were correlated in 34 patients with GA excretion; patients not receiving known enzyme inducers showed low GA values but high 6 beta-OHF and 17-OHCS values, however, with a ratio of 6 beta-OHF/17-OHCS in the normal range. Patients receiving high dose pentobarbitone treatment failed to exhibit significantly increased 6 beta-OHF and 17-OHCS or 6 beta-OHF/17-OHCS values. Miconazole treatment resulted in a significantly increased ratio of 6 beta-OHF/17-OHCS. gamma-Glutamyltranspeptidase activity in serum showed no correlation with GA excretion (n = 91).

17-Hydroxycorticosteroids↗
PubMed1998

Exaggerated urinary excretion of aquaporin-2 in the pathological state of impaired water excretion dependent upon arginine vasopressin.

The present study was undertaken to determine whether urinary excretion of aquaporin-2 (UAQP-2) is of value to diagnose the pathological state of water retention and hyponatremia. UAQP-2 under ad libitum water drinking was 429 fmol/mg creatinine in the patients with water retention, a value significantly greater than that of 153 fmol/mg creatinine in the normal subjects. An acute oral water load test (20 mL/kg BW) was performed in 7 normal subjects (22-25 yr old) and 10 patients with water retention and hyponatremia (55-75 yr old). The percent excretion of the water load was only 30% in the patient group compared with 70% in the control group (P < 0.01). In the control group, minimal urinary osmolality was as low as 131 mosmol/kg H2O, which was responsible for the decrease in plasma arginine vasopressin (AVP) levels after the reduction in plasma osmolality. In the patient group, minimal urinary osmolality was 320 mosmol/kg H2O, and free water clearance remained below 0.6 mL/min after the water load. This impaired water excretion was consistent with the nonsuppressible levels of plasma AVP despite hypoosmolality. The nadir of UAQP-2 was obtained at 60-90 min. The minimal UAQP-2 was reduced to 284 fmol/mg creatinine, a value significantly greater than that of 76 fmol/mg creatinine in the control group. Similar results were obtained in the 6 patients with hypopituitarism, who had impaired water excretion and marked hyponatremia. Water excretion was totally normalized after the replacement of hydrocortisone (excretion of water load, 31% vs. 102%; P < 0.01). Hydrocortisone replacement also significantly reduced the minimal UAQP-2 from 225 to 49 fmol/mg creatinine after the acute oral water load, a value comparable to that in the control subjects. These results indicate that UAQP-2 is a potent marker to diagnose the pathological state of impaired water excretion and hyponatremia, dependent upon AVP, in patients with water retention and hypopituitarism.

Adult↗
PubMed1997

Pulsatile urea excretion in the toadfish (Opsanus beta) is due to a pulsatile excretion mechanism, not a pulsatile production mechanism

When subjected to a crowding/confinement protocol in the laboratory, toadfish become facultatively ureotelic, excreting approximately 90 % of their nitrogenous waste as urea-nitrogen (urea-N). The great majority of this excretion occurs via large, irregular pulses from the head region which occur on average once per day, with a duration of 3 h or less. Pulses measured chemically by the appearance of urea-N in the external water were identical to those measured by assaying [14C]urea appearance in the water from the blood plasma. Individual toadfish maintained plasma urea concentrations over widely differing ranges (6600&shy;39 890 &micro;mol-N l-1). However, independent of absolute levels, both [14C]urea and total urea were distributed at ratios close to unity between the blood plasma and the water compartments of liver and white muscle. At times of pulsatile excretion, plasma urea concentration fell sharply. These decreases, distributed throughout the tissues of the whole body, closely matched the sizes of the measured excretion pulses. Between pulses, plasma urea concentration increased steadily at a much slower rate; the rate of rise, when distributed throughout the tissues of the whole body, corresponded to the time-averaged excretion rate over the whole day. Infusion of a typical pulse amount of urea immediately after the end of a natural pulse event raised plasma urea concentration slightly above the pre-pulse level, but did not induce another pulse event. Plasma cortisol levels declined by approximately 60 % over the 4 h period prior to a natural pulse event and then rose quickly again once the pulse had occurred. These results indicate that urea pulses are due to activation of an excretion mechanism that rapidly clears urea from the blood plasma, thereby lowering stores throughout the whole body. Metabolic production of urea is continuous and is not responsible for pulsatile excretion. The pulse event is not triggered by a specific plasma urea threshold, but may involve the hypothalamo&shy;interrenal axis.

Journal Article↗
PubMed1985

Urinary excretion of plasma proteins in diabetic subjects. Increased excretion of kappa light chains in diabetic patients with and without proliferative retinopathy.

The urinary excretion of beta2-microglobulin, albumin, kappa light chains, transferrin, and IgG as well as their concentration ratios were assessed in 27 nondiabetic patients with proteinuria and in 72 IDDM patients, 41 with proliferative retinopathy (PR) and 31 without retinopathy, matched for age, duration of diabetes, and treatment. The mean excretions of albumin, transferrin, and IgG were similar in patients with nondiabetic proteinuria and in IDDM patients with PR and were significantly higher than in IDDM patients without retinopathy. Despite similar albumin excretion, the amount of excreted kappa light chains was significantly higher in IDDM patients than in patients with nondiabetic proteinuria, resulting in an elevated kappa chain/albumin ratio. Furthermore, diabetic subjects without microalbuminuria showed increased kappa chain/albumin ratio, indicating that increased urinary excretion of kappa chains may be an early sign of diabetic nephropathy. Determination of kappa light chain excretion may have clinical implications in the differentiation between proteinuria of diabetic and nondiabetic origin. The ratio kappa chain/albumin was independent of the excretion of beta2-microglobulin in patients with PR, suggesting that the reduced ability to reabsorb immunoglobulin light chains may occur earlier than that of beta2-microglobulin in the development of tubular dysfunction in insulin-dependent diabetes mellitus.

Adolescent↗