[The modification of kidney function by fat infusion in chronic kidney insufficiency].
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Aminohippuric Acids↗
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Finerenone and Cardiovascular Outcomes According to Baseline Kidney Function in Patients With Heart Failure: The FINEARTS-HF Trial.
BACKGROUND: Finerenone is known to reduce the risk of worsening heart failure (HF) events and cardiovascular (CV) death in patients with HF with mildly reduced or preserved ejection fraction. OBJECTIVES: The authors explored whether the benefit of finerenone among patients with HF with mildly reduced or preserved ejection fraction differs according to baseline measures of kidney function. METHODS: FINEARTS-HF (Finerenone Trial to Investigate Efficacy and Safety Superior to Placebo in Patients With Heart Failure) was a global, randomized clinical trial of finerenone vs placebo among patients with HF with mildly reduced or preserved ejection fraction. Finerenone was titrated to 20 mg/d if the estimated glomerular filtration rate (eGFR) was ≤60 mL/min/1.73 m2 or 40 mg/d if eGFR was >60 mL/min/1.73 m2. The authors used a semiparametric proportional rates method, stratified by left ventricular ejection fraction (<60%; ≥60%) and region, to assess for differential treatment effects on the composite of total HF events and CV death according to the baseline eGFR (continuous and categories [≥60 mL/min/1.73 m2, 45 to <60 mL/min/1.73 m2, <45 mL/min/1.73 m2] and urine albumin-creatinine ratio (UACR) (<30 mg/g, 30 to <300 mg/g, ≥300 mg/g). RESULTS: The effect of finerenone to reduce the primary endpoint of total HF events and CV death did not significantly differ according to baseline eGFR (Pinteraction = 0.14 and 0.07 for continuous and categorical eGFR, respectively) with rate ratio 0.72 (95% CI: 0.59-0.88) for eGFR ≥60 mL/min/1.73 m2, 0.83 (95% CI: 0.65-1.06) for eGFR 45 to <60 mL/min/1.73 m2, and 1.02 (95% CI: 0.83-1.26) for eGFR <45 mL/min/1.73 m2. The corresponding absolute event rates were 9.2 vs 12.5, 16.5 vs 19.9, and 28.0 vs 28.0 per 100 patient-years for finerenone vs placebo, respectively. Similar results were noted for total worsening HF events. Finerenone lowered the risk of the composite CV outcome similarly across baseline categories of UACR (Pinteraction = 0.48). CONCLUSIONS: In the FINEARTS-HF trial (where the target dose of finerenone was determined by baseline kidney function), the effect of finerenone to reduce the composite of cardiovascular death and total HF events did not significantly differ across a range of baseline eGFR and UACR.
Humans↗
Strain differences in kidney function of inbred rats: 1. Glomerular filtration rate and renal plasma flow.
Bodyweight, kidney weight and glomerular filtration rate showed significant differences between strains--70% of the total variance was ascribed to the between-strain variance component--while the renal plasma flow showed only a slight strain difference due to a high within-strain variance component (63%). Heritability in the broad sense was 0.78 for bodyweight, 0.85 for kidney weight, 0.66 for glomerular filtration rate and 0.35 for renal plasma flow. There were significant genetic correlations between bodyweight and kidney weight (0.90), bodyweight and glomerular filtration rate (0.73), and between glomerular filtration rate and renal plasma flow (0.71), but not between kidney weight and kidney functions. Significant environmental correlations could be calculated only between bodyweight and all other variables, so that for comparison between strains it seems better to correct renal functions for bodyweight than for kidney weight, which would increase the variation of glomerular filtration rate.
Animals↗
Changes in kidney function and faecal excretion of water and electrolytes with sodium chloride loading in sheep.
The renal and faecal routes of water and electrolyte excretion in sheep were compared and changes in kidney function assessed when similar amounts of sodium chloride (NaCl) were dosed in free and fixed ratios in water. Sheep (n = 6) either had free access to fresh drinking water (control phase) or 0.9% saline drinking water, or NaCl was dosed intraruminally with free access to fresh drinking water. In the final phase of the investigation, sheep were dosed intraruminally with NaCl while water intake was restricted. Variables monitored included fresh or saline water intake, water, sodium and potassium loss via the urine and faeces, glomerular filtration rate (GFR), fractional excretions of sodium (FENa) and potassium (FEK) and solute free water clearance (CH2O). Results indicated that where NaCl intake was high, sodium excretion via the urine was of far greater importance than that via the faeces and that changes in kidney function which occurred in order to excrete excess sodium, included increases in GFR and FENa, and declines in FEK and CH2O. Where significant differences were obtained in variables between the phases of high salt intake, these were attributed to differences in sodium absorption from the gastrointestinal tract. It was concluded that when NaCl intake is high, sodium homeostasis is chiefly maintained by increasing the amount of sodium made available to the nephron tubule (increased GFR), by decreased tubular reabsorption of this sodium and by increasing solute free water reabsorption.
Animals↗
Long-term effect of lisinopril and atenolol on kidney function in hypertensive NIDDM subjects with diabetic nephropathy.
The aim of our study was to evaluate whether inhibition of ACE (lisinopril 10-20 mg/day) can reduce the rate of decline in kidney function more than reducing blood pressure with conventional antihypertensive treatment (atenolol 50-100 mg/day), usually in combination with a diuretic. We performed a prospective, randomized, parallel study for 42 months, double blind for the first 12 months and single blind thereafter. Forty-three (21 lisinopril and 22 atenolol) hypertensive NIDDM patients with diabetic nephropathy were enrolled. Data from 36 patients (17 lisinopril and 19 atenolol, 60 +/- 7 years of age, 27 men) who completed at least 12 months of the study period are presented. At baseline, the two groups were comparable: glomerular filtration rate (51Cr-EDTA plasma clearance) was 75 +/- 6 and 74 +/- 8 ml x min(-1) x 1.73 m(-2), mean 24-h ambulatory blood pressure (A&D TM2420) was 110 +/- 3 and 114 +/- 2 mmHg, and 24-h urinary albumin excretion rate was 961 (range 331-5,727) and 1,578 (476-5,806) mg/24 h in the lisinopril and atenolol groups, respectively. The mean follow-up time was similar, 37 and 35 months in the lisinopril and atenolol groups, respectively. Mean ambulatory blood pressure was equally reduced in the two groups, 12 +/- 2 and 10 +/- 2 mmHg in the lisinopril and atenolol groups, respectively. Glomerular filtration rate declined in a biphasic manner with a faster initial (0 to 6 months) change of 1.25 +/- 0.49 and 0.81 +/- 0.29 ml x min(-1) x month(-1) followed by a slower sustained decline (6 to 42 months) of 0.59 +/- 0.10 and 0.54 +/- 0.13 ml x min(-1) x month(-1) in the lisinopril and atenolol groups, respectively. No significant differences were observed in either initial or sustained decline in glomerular filtration rate between the two groups. Urinary albumin excretion was reduced (% reduction of baseline) more in the lisinopril than in the atenolol group, at 55 (95% CI 29-72) and 15% (-13 to 34), respectively (P = 0.01). In conclusion, the relentless decline in kidney function characteristically found in hypertensive NIDDM patients with diabetic nephropathy can be reduced equally effectively by two antihypertensive treatments, the beta-blocker atenolol and the ACE inhibitor lisinopril.
Aged↗
Pyeloureteral dynamics. Pelvic pressure and kidney function in partial long-term ureteric obstruction.
In 10 pigs with reno-scintigraphically proven normal upper urinary tracts, a standardized partial obstruction of the left ureter was created at the lower kidney pole level. Three weeks later kidney function was scintigraphically reassessed and the pressure flow relationship in the flow range 0-20 ml/min outlined. The partially obstructed pelvic baseline pressure varied from 9.0 to 32.0 cmH2O. During perfusion small increases in pelvic pressure were seen at all flow rates in the individual cases and there was a linear relationship between pressure and flow. Compared to previous results of a similar but acute obstruction the results were identical in pressure ranges and pressure flow profile. This demonstrates, that a longitudinal stability in transport mechanism qualities is present also during the course of obstruction. The pelvic pressure at low flow rates was significantly correlated to kidney function depression, whereas perfusion pressures at high flow rates did not show any correlation, except at 20 ml/min. This clearly indicates, that the pelvic pressure at normal urine flow rate is an important factor in the pathogenesis of obstructive nephropathy.
Animals↗
Urinary retinol excretion and kidney function in children with shigellosis.
BACKGROUND: Acute infections, including diarrhea, are associated with an increased risk of vitamin A deficiency. Urinary retinol excretion during such infections may contribute to this risk. The mechanism accounting for urinary retinol loss has not been clearly defined. OBJECTIVE: This study attempted to determine whether urinary retinol loss in children with acute infection is associated with impaired kidney function, particularly impaired tubular protein reabsorption. DESIGN: Urinary retinol excretion and kidney function were examined in 66 hospitalized children 5 mo to 5 y of age with acute Shigella dysentery. RESULTS: Urinary retinol loss occurred in 59% of children and was substantial (>0.1 micromol/d) in 8% of them. Children with more severe disease excreted higher concentrations of urinary retinol; those with a body temperature > or =40 degrees C excreted a mean of 0.10 +/- 0.18 micromol/d compared with 0.005 +/- 0.008 micromol/d for other children (P < 0.0001). Children with more severe disease also had impaired tubular reabsorption of low-molecular-weight proteins beta2-microglobulin and retinol binding protein (RBP)], although other measures of tubular and glomerular function were not similarly impaired. In multiple regression analysis, severity of disease indicators were the best predictors of tubular reabsorption of beta2-microglobulin (R2 = 0.53) whereas tubular reabsorption of beta2-microglobulin and RBP were found to be the best predictors of urinary retinol loss (R2 = 0.69). CONCLUSIONS: A significant amount of retinol was excreted in the urine in children with shigellosis: 8% excreted >0.10 micromol/d (15% of the daily metabolic requirement). Impaired tubular reabsorption of low-molecular-weight proteins, such as RBP transporting retinol, appeared to be the cause of this urinary retinol loss.
C-Reactive Protein↗
[Improved kidney function with intravenous prostaglandin E1 in patients with terminal heart failure].
In end stage congestive heart failure activation of a series of compensatory mechanisms increase renal vascular resistance and impair renal function. Prostaglandin E1 is increasingly used in the treatment of severe heart failure for its vasodilating actions. In various experimental settings prostaglandin E analogues are known to improve renal function by modulating renal filtration pressure and redistribution of renal blood flow. However, prostaglandin E1 decreases systemic blood pressure and thus, also renal perfusion pressure, a fact by which renal function might be further compromized in heart failure patients. The aim of the study was to evaluate the effects of prostaglandin E1 on excretory renal function in patients with end stage heart failure and to prove the hypothesis, that the well known local actions of prostaglandins on renal microcirculation might outweigh the negative impact of an expected decrease in perfusion pressure. 25 patients with terminal congestive heart failure were investigated. 13 patients received prostaglandin E1 at a dose of 13.5 +/- 1.9 ng/kg/min in combination with constant rates of dopamine and dobutamine (group A), 12 patients received prostaglandin E1 at a dose of 10.3 +/- 1.7 ng/kg/min without catecholamines (group B). There was no significant difference in prostaglandin dosages between groups. Kidney function was assessed by measuring plasma creatinine and urea nitrogen, urinary output, creatinine clearance, osmotic and free water clearance at baseline and after 72 h of infusion therapy. Hemodynamic parameters were measured by using a balloon tipped pulmonary arterial catheter. Hemodynamic measurements during infusion showed a significant improvement in all patients. At the same time as expected mean arterial pressure decreased in both groups (p < 0.001). Nevertheless, in both groups a significant increase of creatinine clearance during infusion was observed (in group A from 45 ml/min to 78 ml/min., p < 0.05, in group B from 59 ml/min to 105 ml/min., p < 0.001). Creatinine clearance in group B (without catecholamines) reached higher levels than group A (p < 0.05). Urinary volumes did not change during infusion therapy, whereas free water clearance significantly decreased, as an indication of an improvement of renal concentrations ability. We conclude, that in patients with end stage heart failure continuous infusion of prostaglandin E1 improves excretory kidney function. These findings suggest that the local effects of prostaglandin E1 on renal microcirculation can counterregulate the negative impact of prostaglandins on renal perfusion pressure.
Alprostadil↗
[Animal experimental studies on partial kidney function after temporary tourniquet ischemia with and without blood substitute therapy].
70 rats were subjected to tourniquet ischemia of a hind limb for a period of two and three hours. 12 rats served as controls. After release of the 3 hours tourniquets 20 rats were treated either with Ringer's solution or with hydroxyethyl starch. Kidney function and morphology, systolic blood pressure, hematocrit, serum electrolytes, creatinine and urea were studied as different times of recirculation. 1. Reduction in renal function was only observed after releasing the tourniquets. 2. The extent of reduction in renal function depended on the time of ischemia and time of recirculation. 3 hours of tourniquet with two hours of recirculation led to the largest extent of reduction in renal function and renal parenchymal lesions. 3. If the infusion of HES was applied at the beginning of recirculation, reduction in renal function was prevented, as well as parenchymal lesions. Ringer's infusion, however, did not improve kidney function to a normal range.
Animals↗
Focal sclerosis of hypertrophied glomeruli in solitary functioning kidneys of humans.
Morphometric data on glomerular size are presented on three patients with solitary functioning kidneys and one with bilateral oligomeganephronic hypoplasia. Renal biopsy of each of two patients with a congenitally absent kidney (unilateral renal agenesis) and a patient with oligomeganephronie, all with proteinuria and renal insufficiency, reveal increases of mean glomerular diameters of at least 1.75X and mean glomerular volumes greater than 5X. These dimensions, which are in the range of maximal increases recorded for man, are associated in all three biopsies with focal sclerosis of the hypertrophied glomeruli. By contrast, the functionally fully-compensated solitary kidney of a patient who lost function of the contralateral kidney from acquired disease, is characterized by the absence of focal glomerulosclerosis and by glomerular enlargement of significantly lesser degree (increased mean diameter 1.24X and mean volume less than 2X). These observations correlate glomerular injury with glomerular size and suggest that in the setting of reduced nephron numbers, nephron destruction via focal glomerulosclerosis may be initiated when compensatory glomerular hypertrophy has reached its limits.
Adult↗
Combination perfusion-cold storage for optimum cadaver kidney function and utilization.
Dog kidneys were perfused with a newly developed perfusate containing adenosine and PO4 for 48 hr, stored in the same perfusate for an additional 24 hr without perfusion (total preservation time:72 hr), and transplanted with immediate contralateral nephrectomy. Posttransplant renal function and biochemical analysis of the kidneys revealed practically no additional preservation-induced damage during the cold storage period. Serum creatinine levels reached normal between the third and eighth day posttransplant. This preservation method may be the method of choice for patients receiving postoperative cyclosporine therapy--and, in addition, facilitate organ sharing between transplant centers, thus reducing wastage of cadaveric kidneys.
Animals↗
Pharmacodynamics and kinetics of etozolin/ozolinone in hypertensive patients with normal and impaired kidney function.
The effect on urinary electrolyte excretion, renin release and plasma norepinephrine of single oral doses of 400 mg etozolin (E) and of 40 mg furosemide (F) were studied in hypertensive patients with normal (n = 6) and impaired kidney function (n = 6). E caused a marked saluresis up to 24 hours, showing its long duration of action. F, however, displayed a brief, brisk peak diuresis, followed by a rebound from the 4th to the 24th hours. The brisk peak diuresis induced by F was associated with pronounced release of renin, almost twice that induced by E. In chronic renal failure the renin release in relation to the magnitude of the diuresis was increased, i.e. the sensitivity of these patients to changes in water homeostasis was increased. E and F stimulated the sympathetic system to roughly the same extent. Patients with essential hypertension had higher plasma levels of norepinephrine than hypertensive patients with chronic renal failure. In addition, hypertensive patients with normal renal function (n = 4) and varying degrees of renal impairment (n = 11) were also given 400 mg daily for 2 weeks. Effects on blood pressure and electrolyte homeostasis were monitored, as well as the plasma kinetics of metabolite I, ozolinone. At the end of the 2 week treatment E had significantly lowered systolic (-12 mm Hg) and diastolic (-9 mm Hg) blood pressure, and had produced a significant loss of body weight, without altering plasma electrolytes or blood chemistry. There was no accumulation of the effective metabolite ozolinone under conditions of severe impairment of kidney function.(ABSTRACT TRUNCATED AT 250 WORDS)
Adult↗
Kidney function during arterial chemoreceptor stimulation. III. Long-lasting inhibition of renal tubular sodium reabsorption due to pharmacologic stimulation of the peripheral arterial chemoreceptors with almitrine bismesylate.
The reactions of the mean systemic arterial blood pressure, arterial acid-base balance kidney function (clearance-technique), and plasma aldosterone concentration (radio-immunoassay) elicited by stimulation of the peripheral arterial chemoreceptors with almitrine bismesylate were determined in chloralosed, non-vagotomized, spontaneously breathing cats in moderate mannitol-saline diuresis. The left renal nerves were cut; urine was collected separately from both the innervated and denervated kidneys. Intravenous injection of 0.2 mg/kg of the drug caused the expected long-lasting increase of the pO2 and pH and a decrease of pCO2 in the arterial blood, whereas the mean systemic arterial blood pressure slightly rose by an average of 2-4 mm Hg in the first hour of chemoreceptor stimulation but afterwards considerably decreased below the pre-injection values. The renal responses were characterized by a moderate vasoconstriction particularly in the innervated kidneys and a pronounced increase of sodium and urine excretion especially in the denervated kidneys. The inhibition of renal tubular sodium reabsorption underlying these natriuretic and diuretic reactions was fully demonstrable even at the end of the experiments, i. e. 4 h after the administration of the agent. Plasma aldosterone increased with the time of the experiments but did not show any clear relationships to the activity of the arterial chemoreceptors. The results show that the intravenous injection of almitrine bismesylate is connected with a renal response pattern which is typical for an excitation of the peripheral arterial chemoreceptors, i. e. moderate vasoconstriction (efferently mediated by the renal nerves) and an inhibition of renal tubular sodium reabsorption (efferently mediated by hormonal mechanisms). Furthermore, the data suggest that, on the one hand, under certain conditions these reactions of the kidney function could play the role of undesirable side effects but, on the other hand, the inhibition of renal tubular sodium reabsorption caused by almitrine bismesylate might possibly be used to treat diseases that are connected with a reduced ability of the kidneys to sufficiently excrete sodium.
Aldosterone↗
Erythropoietin deficiency causes anemia in nephrotic children with normal kidney function.
Anemia in persistent nephrotic syndrome (NS) has been described in a few case reports but has not been studied systematically. We present a group of 19 children with NS who developed anemia before the deterioration of kidney function. The aim of our study is to determine whether erythropoietin (EPO) and/or iron deficiency are causative factors and to evaluate the effect of EPO replacement therapy. Serum EPO levels, iron status, and vitamin B(12) concentrations were measured in nephrotic patients with anemia (NS-A) and compared with those of nephrotic children with normal hemoglobin (Hb) levels (NS-NHb; n = 13). Two control groups consisted of age-matched patients without kidney disease or hypoxemia with either iron deficiency anemia (IDA; n = 19) or normal Hb concentrations (NHb; n = 16). Most NS-A patients experienced persistent steroid-resistant NS, whereas most NS-NHb children had steroid-responsive NS. Although serum iron, ferritin, and B(12) levels were significantly lower in NS-A children, appropriate replacement therapy that resulted in normalization of ferritin and/or cobalamin levels did not lead to correction of the anemia. NS-A patients had greater EPO levels than those without anemia (21.6 +/- 3.3 versus 5.5 +/- 0.8 IU/L; P: < 0.001), but their response to anemia was inappropriately low compared with IDA children (EPO, 94.6 +/- 15.1 IU/L) despite similar Hb concentrations. EPO therapy for 4 to 9 months in 6 NS-A children with Hb levels less than 9 g/dL led to resolution of the anemia. In conclusion, anemia is a common feature of persistent NS that develops before the deterioration of kidney function. Depletion of iron stores may contribute to the development of anemia, but iron replacement therapy is ineffective. Nephrotic patients have EPO deficiency with a blunted response to anemia. The EPO deficiency is amenable to EPO therapy, which is recommended for this group of patients.
Adolescent↗
Absolute 24 h quantification of 99Tcm-DMSA uptake in patients with severely reduced kidney function: a comparison with 51Cr-EDTA clearance.
The aim of this study was to determine whether absolute 24 h DMSA uptake measurements (%DMSA) correlate well with 51Cr-EDTA clearance measurements in patients with severely reduced kidney function (SRKF). Between 1990 and 1997, 55 of 482 patients who underwent EDTA clearance measurements also underwent %DMSA within 1 week. Of these, 31 were women and 24 were men (mean age 60 years; range 19-77 years). EDTA clearance was determined using the slope-intercept method. Absolute depth- and background-corrected %DMSA were determined 24 h following the injection of 185 MBq per 1.73 m2 freshly prepared 99Tcm-DMSA. All patients had EDTA clearance < or = 60 ml.min-1. Eighteen patients (group A: 9 men and 9 women, mean age 55.8 years, range 28-73 years) had EDTA clearance > 20 ml.min-1 (mean +/- S.D. = 30.9 +/- 13.8 ml.min-1), whereas 37 patients (group B: 22 women and 15 men, mean age 62.0 years, range 19-77 years) had EDTA clearance < 20 ml.min-1 (mean +/- S.D. = 10.2 +/- 6.6 ml.min-1). EDTA clearance correlated well with %DMSA for the patients as a whole and for group A (r = 0.87, P = 0.73; r = 0.79, P = 0.0001 respectively). The regression equation suggests that %DMSA is not a marker of early renal dysfunction. In group B, the r-value (r = 0.48, P = 0.004) suggests that %DMSA is reliable as a marker of severe renal dysfunction to the extent that it provides rough information. In conclusion, %DMSA may not be used as a marker of early renal impairment. Additionally, in patients with severely reduced kidney function (EDTA clearance < 20 ml.min-1), it only provides a rough estimate.
Adult↗
[Lithium treatment and kidney function].
Systematic cross-sectional and longitudinal examinations of the kidney function of patients in prophylactic lithium treatment have established that the therapy, even when given for many years, does not affect the glomerular filtration rate or lead to kidney failure. Lithium treatment may induce polyuria and lowered renal concentrating ability, but these side effects do not presage deterioration of the filtration rate, and they are not dangerous if dehydration is avoided. It is now possible to revise and simplify the guidelines for laboratory monitoring of maintenance treatment with lithium.
Bipolar Disorder↗
A longitudinal study of the kidney function of the chimpanzee (Pan troglodytes) in comparison with humans.
A prospective study of the kidney function of chimpanzees (Pan troglodytes) kept at the Hans Popper Primate Centre has been performed within the last 10 years. The aim of the study was to analyse urine samples for specific gravity, to determine serum creatinine, serum urea, and urinary creatinine, and to calculate creatinine clearance and reference values for healthy chimpanzees. From 1750 urine specimens of adolescent and 568 of infant chimpanzees a mean specific gravity value of 1.013 +/- 0.006 (standard deviation) kg/l and 1.007 +/- 0.003 (standard deviation) kg/l, respectively, was calculated. Serum creatinine was determined in 1864 single samples from 52 chimpanzees; a median value of 101.8 mumol/l (P (5%) 79.6 mumol/l, P (95%) 139.7 mumol/l) was calculated, which is higher than that in humans. Serum urea tests (n = 1831) in the same 52 chimpanzees resulted in a median value of 2.01 mmol/l (P (5%) 0.86 mmol/l, P (95%) 4.78 mmol/l). The calculated median creatinine clearance value of 23.9 ml/min (P (5%) 4.4 ml/min, P (95%) 65.3 ml/min) is lower in chimpanzees than in man. A correction of the creatinine clearance values to the body surface area of 1.73 m2, as routinely performed in humans, gave unusually high results, as there was no proper equation to calculate the surface area of chimpanzees. The use of estimation equations for creatinine clearance values of chimpanzees as developed for humans is therefore not recommended.
Animals↗
Diminished kidney function and nephrocalcinosis in rats fed a magnesium-deficient diet.
The effect of a magnesium-deficient diet on kidney function was studied in young male rats. The rats were fed a purified diet with a magnesium content of either 20.5 (control diet) or 2.6 mmol/kg (magnesium-deficient diet) for 21 d. In rats fed the magnesium-deficient diet, kidney wet and dry weights were significantly increased, and calcium and phosphorus concentrations in the kidney were significantly higher than in rats fed the control diet. Upon histological examination, an increase in the mesangial matrix of the glomeruli and injury to the brush border of the proximal tubules were observed in rats fed the magnesium-deficient diet. Also, a deposition of calcium was observed in the tubules of the corticomedullary junction and medulla of these rats. Total protein and albumin concentrations in serum were significantly decreased in rats fed the magnesium-deficient diet. Urinary albumin excretion was significantly higher, and N-acetyl-beta-D-glucosaminidase activity in the urine was significantly increased in rats fed the magnesium-deficient diet. These findings indicate diminished glomerular and proximal tubular functions. We suggest that a magnesium-deficient diet not only induces nephrocalcinosis, but it also diminishes kidney function.
Acetylglucosaminidase↗