Several homeostatic renal functions in hypertensive and nephrotic syndromes of chronic functionally compensated glomerulonephritis

Homeostatic renal functions in nephrotic syndrome (NS) and arterial hypertension were studied the data on 240 patients with functionally compensated chronic glomerulonephritis (CGN). Benign arterial hypertension did not make a considerable effect on renal functions. In NS there was a selective decrease in the functions, particularly affected in the tubulointerstitial component (TIC) of CGN (concentration and ammonium secretory functions). These functions were affected to the maximum in proteinuria over 9.0 g/day. The NS adverse effect on renal transport processes was not dependent on the TIC presence. In CGN accompanied by moderate proteinuria, even a moderate decrease in renal concentration function or a considerable decrease in ammonium secretory function suggested the TIC presence. Against a background of the NS the presence of CGN TIC could be supposed only in the detection of maximum urine osmolarity not exceeding 600 mmol/l.     

Lipiduria in the nephrotic syndrome]

A study was made of urine lipids and their fractions in chronic glomerulonephritis (CGN) and renal amyloidosis with nephrotic syndrome (NS). 91 patients suffering from NS were examined. 2 subgroups were distinguished among these patients: with CGN of the nephrotic type and with the nephrotic stage of renal amyloidosis. The reference groups were made up of patients with latent CGN and healthy subjects. Measurements were made in the blood and urine of total lipids (TL) and their fractions--phospholipids (LP), free cholesterol (FC), mono- and diglycerides, triglycerides (TG), and cholesterol esters (CE). The presence of the NS was attended by a rise in the blood of TL concentration, relative content of FC, TG and by a decline of RL and CE, with the decrease of the relative content being more manifest in amyloidosis. Nephrotic lipiduria was largely characterized by an increase of the concentration of TL and of the relative content of PL, with the changes of the latter parameter being mostly characteristic of CGN patients. Thus, NS was associated with a high excretion of lipids with urine which is likely to reflect their elevated filtration under nephrotic hyperlipidemia. Still, in nephropathies whose pathogenesis is determined by an important role of inflammatory and membrane-destructive processes, of definite role is also the local (renal) formation of PL.     

Clinical significance of nitric oxide levels in patients with chronic glomerulonephritis

Nitric oxide (NO) takes an active part in the regulation of the main renal functions, water-salt metabolism, and system arterial pressure. Under pathological conditions, NO plays the leading role in the development and progression of nephrosclerosis. The aim of this study was to evaluate the clinical significance of serum and urine levels of stable NO metabolites in patients with various clinical forms of chronic glomerulonephritis (CGN), as well as CGN patients with chronic renal failure (CRF). Ninety-seven CGN patients, including 56 ones with preserved nitrogen excretion and 41 ones with CRF, were examined. The levels of stable NO metabolites (nitrites and nitrates) in serum and 24-hour urine were measured. The highest serum and urine NO levels were found in patients with nephrotic and hematuric CGN; patients suffering from latent and hypertonic CGN displayed the lowest levels. Patients with CRF had higher serum levels of NO compared with non-CRF patients. A reverse correlation between serum levels of creatinine and NO in patients with CRF was revealed. In CGN patients without CRF, the activity of inflammatory process, observed by high C-reactive protein levels, was associated with elevation of blood and urine levels of NO, while such an association was not found in patients with CRF.     

Urinary fibronectin as an indicator of kidney fibrosis in nephritis]

AIM: To investigate clinicomorphological relationships between elevated urinary excretion of fibronectin (FN) and development of fibrosis in the kidney in patients with lupus nephritis (LN) and chronic glomerulonephritis (CGN). MATERIALS AND METHODS: Urinary FN excretion was measured at radial immunodiffusion in 54 LN patients. Of them, 15 patients had inactive LN, 39 patients had active LN varying in clinical forms. Urinary FN was also measured by passive hemagglutination in 36 CGN patients (11 inactive CGN and 25 active CGN cases). Biopsy specimens were obtained from 49 patients with active nephritis (43 with CGN and 6 with LN). FN deposits were studied immunohistochemically and morphometrically with determination of relative fibrosis area. RESULTS: Urinary FN excretion in patients with nephritis was higher than in healthy controls. In active CGN and LN the levels of FN were significantly higher than in inactive CGN and LN. The highest FN urinary concentrations were registered in patients with severe CGN and LN, especially in the presence of renal failure and arterial hypertension. Among them, the highest individual values were observed in patients with rapidly progressive nephritis. No positive correlations were found between the degree of the urinary FN excretion increment and degree of proteinuria. This suggests local-renal origin of most urinary FN. Morphologically, FN deposits were revealed in 73% of the biopsies. In most of the patients with severe nephritis both in CGN and LN there was a diffuse distribution of FN in the glomerules and interstitium. A correlation with a morphological nephritis type was absent, but existed between FN presence in the renal biopsies and relative area of interstitium (fibrosis). CONCLUSION: FN excreted in high amounts with urine in nephritis originates from the kidneys and reflects severity of fibrogenesis in the kidney.     

Urine excretion of a monocytic chemotaxic protein-1 and a transforming growth factor beta1 as an indicator of chronic glomerulonephritis progression

AIM: To measure urine and renal tissue levels of profibrogenic mediators (monocytic chemotaxic protein-1-MCP-1 and transforming growth factor beta1 - TGF-b1) in patients with chronic glomerulonephritis (CGN); to specify significance of these mediators for assessment of inflammation and fibrosis in the kidney and as prognosis criteria. ELISA, immunohistochemical tests, morphometry were used to study urine excretion of MCP-1 and TGF-b1, expression of TGF-b1 in renal tissue, interstitial area, respectively, in 63 patients with active proteinuric CGN. RESULTS: Patients with active proteinuric forms of CGN have higher urine excretion of MCP-1 and TGF-b1 than healthy controls. Urine excretion of MCP-1 in patients with nephrotic syndrome was significantly higher than in patients with moderate urinary syndrome. The highest MCP-1 urine excretion was observed in patients with persistent renal failure. Urine excretion of TGF-b1 depended on the level of creatinemia being the highest in marked proteinuria and stable renal dysfunction. Intensive urine excretion of TGF-b1 occurred in CGN patients with expression of this cytokine in renal interstitium. This confirms its local-renal origin. A correlation was found between urine values of MCP-1, TGF-b1 and severity of tubulo-interstitial fibrosis (TIF). High informative value (sensitivity and specificity) of urine MCP-1 and TGF-b1 are for the first time shown as markers of interstitial fibrosis. They are also important for making prognosis of CGN. CONCLUSION: It is shown that MCP-1 and TGF-b1 are essential for remodeling of tubulointerstitium. The urinary parameters mark TIF and can be used as criteria of activity and prognosis of CGN.     

Clinical implication of urine test for markers of endothelial dysfunction and angiogenesis factors in assessment of tubulointerstitial fibrosis in chronic glomerulonephritis

AIM: To evaluate contribution of endothelial dysfunction and impairment of endothelial proliferation/ regeneration to mechanisms of development of tubulointerstitial fibrosis (TIF) in chronic glomerulonephritis (CGN) basing on urinary levels of markers of endothelial activation/impairment and angiogenesis factors. MATERIAL AND METHODS: A total of 67 CGN patients entered the study: 19 patients with moderate urinary syndrome (group 1), 37 patients with nephrotic syndrome (group 2), 11 patients with nephrotic syndrome and persistent renal failure (RF). A control group consisted of 12 healthy subjects. The examination covered excretion with urine of Willebrand factor (WF), plasminogen activator inhibitor I (PAL-I), fibrin degradation products (FDP), vascular endothelial growth factor (VEGF). These values were compared with severity of fibrous changes in renal interstitium estimated by biopsy morphometry. RESULTS: CGN patients had signs of affection of parietal effects of vascular endothelium. In particular, increased excretion of functionally active WF, PAI-I and FDP correlating with activity/severity of CGN. The changes were especially noticeable in patients with progressive forms of CGN (with NS and RF). Patients with morphologically verified TIF (interstitial area more than 20%) excretion of endothelial dysfunction markers was higher than in CGN patients free of TIF In a progressive course of nephritis endothelial dysfunction deteriorates by endothelial proliferation/regeneration impairment as shown by reduced urinary excretion of angiogenic factor VEGF and parallel elevation of functionally active WF in urine of patients with severe forms of CGN. Combined contribution of endothelial dysfunction and angiogenesis impairment to mechanisms of TIF development is seen from these values relations with severity of creatinemia and fibrous alterations in tubulointerstitial tissues of the kidney. CONCLUSION: The results point to participation of endothelium in mechanisms promoting development of TIF and RF in CGN both in terms of endothelial dysfunction and impairment of endothelial repair capacity. Clinicomorphological comparisons confirm the significance of WF, PAI-I and VEGF in assessment of local-renal endothelial changes and severity of fibrosis in renal tissue in CGN. Due to availability of the study material, perspectives of fibrogenesis monitoring in the kidneys with the tests appear which is essential for making prognosis and treatment policy in CGN patients.     

Tubulointerstitial component of chronic glomerulonephritis. Clinico-morphological comparisons

A total of 179 patients with chronic glomerulonephritis were examined for the development of the tubulo-interstitial component (TIC) of the disease. It was established that the rate of the development and intensity of the TIC are linked with different morphological variants of GN and increase successively in mesangiomembranous, membranous, mesangioproliferative, mesangiocapillary (and lobular) GN, reaching a maximum in diffuse fibroplastic GN. In patients with no TIC, the hematuric and latent forms of CGN were mostly encountered. The disease took a stable course, with a frequent occurrence of improvements and remission. The 5-year survival was 100%. In patients with a moderate TIC, the nephrotic form of CGN was encountered more often than in other patients. As regards other characteristics, this form occupied an intermediate position, with the 5-year survival rate amounting to 91%. Patients with a pronounced TIC were marked by progressive CGN, which was largely observed in the hypertonic and mixed patterns of the disease. The three-year survival amounted to 34% in this case. The TIC of CGN is an important prognostic factor and the dissimilar course of different morphological variants of CGN is accounted, to a considerable degree, for by the dissimilar rate of TIC development.     

Renal bicarbonate reabsorption and hydrogen ion excretion in normal infants

After acute administration of ammonium chloride, infants 1 to 16 months of age were similar to older children in their capacity to acidify their urine. The infants had a higher rate of excretion of titratable acid and a lower rate of excretion of ammonium but were similar in their rate of excretion of total hydrogen ion.     

Possible mechanisms of polyuria in progressive chronic renal failure

AIM: Elucidation of the role of saluresis and osmotic diuresis in renal function of patients with chronic renal failure. MATERIAL AND METHODS: The trial included 68 subjects, among them 25 patients with chronic renal failure (CRF) of the third and fourth degree aged 16 to 72 years. Enzyme immunoassay was used to measure osmolality, sodium, potassium, magnesium, calcium and creatinine concentrations in the serum and urine as well as urine prostaglandin E2. RESULTS: Renal function was studied in CRF patients with a 75-90% fall of glomerular filtration rate. Creatinine clearance was 19.9 +/- 0.96, it varied in different patients from 10.6 to 29.7 ml/min. It is shown that diuresis does not correlate with the total ion excretion (Na+ plus K+)(r = 0.946, p < 0.0001). A correlation was found between excretion of these ions and Mg2+ ions this indicating location of reabsorption reduction in the thick ascending limb of Henle loop. In CRF patients (Na+ plus K+) excretion correlated with PGE2 excretion (r = 0.65, p < 0.0001). CONCLUSION: It is suggested that at this stage of chronic renal failure the mechanism of a diuresis increase is not due to osmotic diuresis but rather to secretion of prostaglandin E2 which inhibits cation reabsorption and stimulates diuresis. Differences are considered between osmotic diuresis and different types of saluresis; their possible mechanisms are discussed.     

Familiar hyperkalaemic acidosis

We evaluated a 26-year-old man with hyperkalaemic acidosis, apparently inherited as an autosomal dominant trait. Type II pseudohypoaldosteronism was suggested by normal aldosterone production and renal sodium conservation. The cause of acidosis in this syndrome is unknown. Both urinary ammonium excretion and bicarbonate threshold were low during hyperkalaemia. After correcting the hyperkalaemia ammonium excretion was normal, but bicarbonate threshold remained low. Maximum bicarbonate reabsorption, urine to blood pCO2 gradients, and minimum urine pH were normal. These findings suggest that hyperkalaemia might contribute to the acidosis by limiting urinary buffer, but that the primary defect is reduced mineralocorticoid effect on hydrogen ion secretion. When the poorly reabsorbed anion, sulphate, was infused, hydrogen ion and potassium secretion were normal. When the relatively reabsorbable anion, chloride, was infused, potassium secretion was decreased. These findings suggest that the attenuated mineralocorticoid effect on hydrogen ion secretion is due to increased reabsorptive avidity for chloride in the distal nephron. To determine if this defect caused resistance to mineralocorticoid we increased mineralocorticoid by dietary sodium restriction and later administered desoxycorticosterone and fludrocortisone. Both endogenous and exogenous mineralocorticoid caused increased net acid excretion and corrected the acidosis, indicating no resistance to mineralocorticoid. Hydrochlorothiazide 50 mg daily promptly corrected the acidosis and the hyperkalaemia by increased urinary potassium excretion. We conclude that the acidosis of type II pseudohypoaldosteronism is due in part to attenuation of the voltage-dependent moiety of mineralocorticoid-driven acidification caused by enhanced distal chloride reabsorption. Suppression of ammoniagenesis by hyperkalaemia exaggerates the acidosis. The acidosis and hyperkalemia are corrected by hydrochlorothiazide.     

Studies on the Pathogenesis of Type I (Distal) Renal Tubular Acidosis as Revealed by the Urinary Pco2 Tensions

This study was designed to investigate the pathogenesis of type I (distal) renal tubular acidosis.Urinary and blood Pco(2) tensions were determined when the pH of the urine was equal to or exceeded the corresponding blood pH. This provided an indication of net hydrogen ion secretion in the distal nephron. In 16 normal subjects, the Pco(2) of the urine exceeded blood values (U-B Pco(2)) by 32.7+/-3.1 mm Hg. In contrast, the urinary Pco(2) tensions in 10 patients with type I (distal) renal tubular acidosis were not significantly greater than blood values (U-B Pco(2) = 2.0+/-2.2 mm Hg). These results indicate that type I (distal) renal tubular acidosis is caused by failure of the cells of the distal nephron to secrete hydrogen ions rather than to gradient-limited hydrogen ion addition to the urine. This is suggested by the fact that urinary Pco(2) levels should be higher than blood Pco(2) levels when hydrogen ions are secreted into urine containing bicarbonate in the distal nephron and they were not in this study despite the presence of a favorable hydrogen ion gradient (tubular fluid pH exceeded blood pH).     

Mineral metabolism during short-term starvation in man

Plasma and urine electrolytes were measured in five healthy non-obese young adults before, during and after a four-day period of total starvation (distilled water only). Plasma sodium, chloride and bicarbonate concentrations decreased in all subjects by a mean value of 4 mmol/l, whereas the sum of acetoacetate and hydroxybutyrate concentrations increased by 4-6 mmol/l. These changes occurred without alterations in the state of hydration or vascular volume. Hydroxybutyrate and ammonium ions became the main urinary ions during starvation, whereas sodium and chloride, which were quantitatively the most important urinary electrolytes before starvation, decreased four-fold, and potassium two-fold. Plasma zinc concentrations rapidly increased in all subjects by a mean of 4 mumol/1 (25%) and returned to normal on refeeding. The excretion of zinc in urine trebled and continued to rise on refeeding. There were no major changes in the excretion of calcium, magnesium, phosphate or sulphate during the starvation period. From knowledge of the intracellular concentrations of various minerals and extent of breakdown of lean tissues (N excretion), it is suggested that most of the urinary calcium, magnesium and phosphate probably originates from bone, and that the amount of zinc in urine is only a small fraction of that which is likely to be released from the breakdown of lean tissues. It is also suggested that the continued excretion of zinc on refeeding is due to release of zinc from tissues which 'buffered' it during the starvation period. This study provides useful data in non-obese individuals with which to compare changes which occur in post-traumatic and post-infective starvation.     

Anemia in diabetic nephropathy: prevalence, clinical and pathophysiological aspects

AIM: To investigate detectability of anemia, its clinical and pathophysiological features in patients with diabetic nephropathy (DN). MATERIAL AND METHODS: The trial included 1020 patients with type 1 and 2 diabetes mellitus (DM). DN was diagnosed in 50% of them. Incidence of anemia was compared in 92 DN patients in type 1 DM and in 230 patients with chronic glomerulonephritis (CGN). Concentration of erythropoietin (EP) in blood serum was measured in 94 DN patients in type 1 and 2 DM. RESULTS: Anemia develops in type 1 and 2 DM patients free of DN and unaffected renal filtration function (glomerular filtration rate--GFR > 60 ml/min 1.73 m2) was 23.3 and 18.3%, respectively. In DN patients incidence rate of anemia depended on GFR and increased with growing severity of renal failure reaching 85.7% in GFR < 30 ml/min/1.73 m2. Development of anemia in DN depended also on protein urine excretion (20.0% in normoalbuminuria, 25.7% in microalbuminuria and 48.2% in proteinuria). Anemia in DN was detected more frequently and was more severe (by hemoglobin reduction) than anemia in CGN in equal GFR. At all stages of chronic disease of the kidneys EP secretion was low normal and independent of Hb and GFR. CONCLUSION: In DN anemia occurs more often and is more severe than in CGN. Anemia results from inadequate production of EP by the kidneys in response to anemia. Thus, early start of its correction is necessary for improvement of quality of life and inhibition of progression of micro- and macrovascular complications of DM.     

Early diagnosis of acute renal insufficiency in patients with peritonitis

Changes in osmolarity, blood and urine levels of medium-size molecules (MSM), osmolarity and MSM index, free water clearance (FWC) and alterations in traditional clinical and biochemical parameters typical of acute renal failure (creatinine, urea nitrogen, K+, Na+, diuresis) have been compared in 27 patients with peritonitis complicated in 17 cases by acute renal failure (ARF). In patients with developing ARF disturbances in osmotic condition, osmotic clearance, FWC, MSM level precede an increase in creatinine and urea nitrogen level and diuresis decrease. Dynamic studies of FWC and MSM blood and urine levels allow of early ARF diagnosis in patients with peritonitis. Progressive growth of plasma osmolarity and FWC with a parallel decrease in MSM index below 1 is a criterion indicative of functional renal failure turning into organic one.     

颈髓损伤后水电解质紊乱的临床诊断治疗

目的 探讨颈髓损伤后电解质紊乱的临床特点及诊断治疗.方法 回顾30例颈髓损伤患者（完全性损伤15例，不完全性损伤15例）血压、心率，血清钠、钾、血浆渗透压、尿量及24ｈ尿钠排出量等资料：23例患者于伤后2－8天出现低钠血症，其中完全性损伤15例全部出现，发生率100％，1例患者并发抗利尿激素分泌异常综合征 结果 根据血钠水平,经采用控制每日水量、补钠治疗5－14天后，23例均治愈,血钠平均恢复至138(135－142)mmol/l,血浆渗透压、尿钠均正常.结论 低钠血症是颈髓损伤后极为常见的并发症，但并发抗利尿激素分泌异常综合征十分少见；机体内抗利尿激素不适当分泌，导致的稀释性低钠血症可能是颈髓损伤继发低钠血症的发生机制之一。严格控制入液量及补钠为主要治疗方法.     

Antibacterial activity of human urine

The fate of bacteria in human urine was studied after inoculation of small numbers of Escherichia coli and other bacterial strains commonly implicated in urinary tract infection. Urine from normal individuals was often inhibitory and sometimes bactericidal for growth of these organisms. Antibacterial activity of urine was not related to lack of nutrient material as addition of broth did not decrease inhibitory activity. Antibacterial activity was correlated with osmolality, urea concentration and ammonium concentration, but not with organic acid, sodium, or potassium concentration. Between a pH range of 5.0-6.5 antibacterial activity of urine was greater at lower pH. Ultrafiltration and column chromatography to remove protein did not decrease antibacterial activity.Urea concentration was a more important determinant of antibacterial activity than osmolality or ammonium concentration. Increasing the urea of a noninhibitory urine to equal that of an inhibitory urine made the urine inhibitory. However, increasing osmolality (with sodium chloride) or increasing ammonium to equal the osmolality or ammonium of an inhibitory urine did not increase antibacterial activity. Similarly, dialysis to decrease osmolality or ammonium but preserve urea did not decrease inhibitory activity. Decreasing urea with preservation of ammonium and osmolality decreased antibacterial activity. Removal of ammonium with an ion exchanger did not decrease antibacterial activity, whereas conversion of urea to ammonium with urease and subsequent removal of the ammonium decreased antibacterial activity.Urine collected from volunteers after ingestion of urea demonstrated a marked increase in antibacterial activity, as compared with urine collected before ingestion of urea.     

肾小管泌氢功能检测在肾移植对抗排斥反应治疗效果中的应用

背景：移植后的急性排斥是肾移植术后的主要并发症，也是导致慢性排斥反应和移植物失功最重要的危险因素，因此，了解肾小管泌氢功能能否早期反映移植物的功能情况有重要意义。目的：观察肾移植患者术后肾小管泌氢功能，并进行监测，探讨其在移植物急慢性排斥中的作用。设计：病例-对照观察。单位：解放军济南军区总医院泌尿外科。对象：选择2000—05／2005—06解放军济南军区总医院泌尿外科连续实施肾脏移植26例患者，男16例，女10例；年龄21～58岁，平均35岁。原发病均为慢性肾小球肾炎，慢性肾功能衰竭，全部为尸肾移植。供受者均血型相同、淋巴细胞毒试验阴性。其中1例为第2次移植。所有患者对检测项目知情同意。方法：依据典型的临床表现，彩色多普勒超声及血流变化诊断患者排斥反应，16例患者未发生排斥反应为稳定组，10例发生排斥反应的患者为排斥组，排斥组根据排斥情况分为排斥前期、排斥期及恢复期。对所有患者术前及术后1周起每周1次，连续10周分别以化学清洁玻璃瓶留取晨起中段尿测定尿可滴定酸、NH4^＋和净酸水平评估肾小管泌氢功能。主要观察指标：两组患者尿可滴定酸、NH4^＋和净酸水平。结果：纳入患者26例均进入结果分析。排斥反应组排斥前期患者肾小管泌氢功能各检测值显示泌氢功能开始建立，并趋向正常，排斥期患者肾小管泌氢功能检测值均显示明显下降，与排斥前期及稳定组比较均有统计学显著性差异（P〈0．01）。恢复期患者排斥反应治疗后监测的结果显示泌氢功能恢复较快。肾小管泌氢功能总体连续观察结果显示总体恢复的不均衡性，大部分病例恢复时间从1～10周不等，平均恢复期限约6周，2例10周内未恢复，4例严重排斥者中3例治疗后泌氢功能恢复缓慢。结论：肾小管泌氢功能可弥补血清肌酐不能良好反映肾小管功能的不足，能在连续观察中对移植肾急性排斥反应的诊断，特别是对抗排斥治疗的效果判断和预后评估中作为有价值的指标。     

Tests for cell membrane destabilization in assessing activity-progression of chronic glomerulonephritis

AIM: To study the role of cell membrane destabilization (MD) in the serum and urine in assessing activity/progression of primary chronic glomerulonephritis (CGN). MATERIAL AND METHODS: The trial entered 163 patients (mean age 38 +/- 7.3 years) with primary CGN in active phase, 64 patients with CGN in remission and 24 controls. The groups were compared by MD (urine phospholipids--PL, blood and urine ethanolamine--EA), indexes of activity and sclerosis (AI and SI), lipid peroxidation (LPO), etc. RESULTS: In active glomerulonephritis (GN) vs inactive one there were high levels of 24-h proteinuria, AI, PL and EA in the urine, malonic dialdehyde (MDA) and hydroperoxides (HP) in the blood. SI was similar in both groups. In active GN significant correlations were found between urinary SI, systolic and diastolic pressure, elevated levels of beta-lipoproteins and triglycerides; between blood EA and 24-h proteinuria, blood platelets, beta-lipoproteins, triglycerides, MDA, urine EA. CONCLUSION: LPO and MD play an essential role in GN pathogenesis. They reflect activity of inflammation in GN irrespective of the activity type and clinicomorphological form of GN, absence or presence of CRF.     

Effect of para-aminohippurate on renal glutamine metabolism in the rat.

After para-aminohippurate (PAH) infusion into rats, urine pH decreased and urine ammonium excretion increased. Because augmented urine flow and decreased urine pH could not explain entirely the enhanced ammonium excretion, an increased ammonia production was postulated as a contributing influence. This was supported by the in vitro findings that PAH could increase slice ammoniagenesis from glutamine. The ability of PAH to stimulate ammoniagenesis in vitro was attributed to enhanced phosphate-dependent glutaminase activity. We conclude that PAH infusions at certain concentrations in vivo can alter ammonium excretion through increased renal ammonia production. The latter may be secondary to enhanced phosphate-dependent glutaminase activity.     

Is the urinary excretion of prostaglandin E in man dependent on urine pH?

The relationship between urine pH, modified by the oral administration of either ammonium chloride or sodium bicarbonate, and the urinary excretion of prostaglandin E (PGE) was studied in healthy female subjects. The urinary concentration of PGE, normally constant in man, was significantly higher (P less than 0.02) in alkaline than in acid urine. pH-dependent metabolism and flow-dependent excretion were identified as two factors liable to obscure the demonstration of the pH-dependency of the urinary excretion rate of PGE in man.