Hypercalcaemia and glucagon-mediated urinary electrolyte excretion in minipigs

Summary The effects of glucagon (G) on glomerular filtration rate (GFR) and the urinary excretion of electrolytes were studied during sequentially increasing hypercalcaemia in minipigs. G has no specific effect on GFR. The observed increase in the excretion of electrolytes was probably due to increased amounts of calcium in the glomerular filtrate rather than to any specific hormonal effects. The results obtained in parathyroid suppression experiments (using i. v. infusion of calcium) suggest that the renal effects of G may somehow be related to intact thyroid-parathyroid activity and normal circulating levels of these hormones.     

A study of urinary immunoglobulins and electrolyte excretion after lordosis]

We described a transient low or non-selective proteinuria after forced lordosis as a characteristic of orthostatic proteinuria and the heteroporous theory and sieving function theory which might explain the mechanism of orthostatic proteinuria. The angiogenic action of the renin-angiotensin system played an important part in these theories. Angiotensin II was recognized as the key regulator of renal sodium excretion, because it reduced the urinary Na/K ratio. Since the purpose of this study is to investigate the influence of the renin-angiotensin system on the mechanism of orthostatic proteinuria, proteins and electrolytes in the urine were examined before and after lordosis in 9 healthy children (Group A) and in 6 children with orthostatic proteinuria (Group B). The urinary ratio of protein/creatinine (P/cre) in Group B was already significantly higher than that in Group A before lordosis and significantly increased after lordosis, while P/cre in group A did not increase after lordosis. The urinary Na/K ratio (Na/K) in Group B was already significantly lower than that in Group A before lordosis, and after forced lordosis, Na/K in Group A decrease with no difference between both groups observed. It is suggested that a significant increase on P/cre after lordosis was obtained only in Group A, whereas in both groups the renal vein may be compressed by forced lordosis and as a result angiotensin II may be stimulated. There might be a difference of the responsibility to angiotensin II in glomerular mesangium contraction between both groups.     

The role of fludrocortisone in a child with cerebral salt wasting

Cerebral salt wasting (CSW) is a syndrome of hyponatremia due to excessive natriuresis described in patients with central nervous system insult. We present a 29-month-old black male with tuberculous meningitis who developed CSW with depressed mineralocorticoid activity. The patient required hypertonic saline and ionotropic support. Mineralocorticoid supplementation effectively treated CSW. Received October 20, 1997; received in revised form and accepted February 18, 1998     

外伤后脑性盐耗综合症合并难控性尿量增多的临床治疗分析

脑性盐耗综合征（cerebral salt wasting syndrome，CSWS）常并发于重型颅脑损伤后，其中部分患者可同时发生难控性尿量增多，常可引起病情的急剧变化，甚至危及生命。本院自2003年1月以来共收治重型颅脑损伤后并发CSWS患者53例．现报告如下。     

Influence of progressive salt restriction on urinary bicarbonate wasting in uremic acidosis

In steady state, the acidosis in the majority of 17 uremic patients was characterized by a persistent bicarbonaturia (FEHCO3 ranging between 0% and 17.65%). An NH4Cl loading test in 17 patients revealed two distinct groups: group A (n = 11) with complete disappearance of the urinary bicarbonate loss and a mean UpH of 5.39 +/- 0.10 at a PHCO3 level of 13.3 +/- 0.5 mEq/L; and group B (n = 6) with urinary acidification disturbances with a persistent FEHCO3 ranging between 1.06% and 3.15% and a mean UpH of 6.53 +/- 0.06 at a PHCO3 level of 13.5 +/- 0.7 mEq/L. Between the two groups, there were no differences in CCr, plasma Na, K, Cl, Ca, PO4, PCO2, and aldosterone levels. Calculation of the THCO3/TNa reabsorption ratio over a wide range of PHCO3 levels revealed no differences between the two groups. The mean levels of circulating PTH were significantly higher in group B compared with group A (40.1 +/- 10.8 mU/dL v 19.3 +/- 4.4 mU/dL; P less than .05), and the spontaneous steady-state FENa was more pronounced in group B than in group A (12.1% +/- 1.5% v 4.9% +/- 0.7%; P less than .05). Four patients from group B with a well-documented salt-losing nephropathy (FENa ranging from 10.20% to 15.10%) were submitted to a progressive dietary salt restriction over several weeks. At this stage, the four patients no longer had bicarbonaturia, and the urinary pH decreased to levels between 5.15 and 5.65 during NH4Cl-induced acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)     

Acute effects of gentamicin on urinary electrolyte excretion in neonates

It has recently been shown that a single dose of gentamicin causes immediate and transient calcium and magnesium renal wasting in adults. The aim of this study was to determine the acute effect of gentamicin administration on renal electrolyte handling in preterm and full-term neonates. Twenty-three neonates treated with gentamicin for suspected infection were enrolled in the study. Serum and 3-h urine electrolytes were measured before and immediately after gentamicin infusion on the 1st, 3rd, 4th, and 7th day of treatment. Serum gentamicin levels were monitored. Gentamicin caused a statistically significant post-infusion increase in fractional excretion of sodium and magnesium and in the urine calcium to urine creatinine ratio. Potassium and phosphate fractional excretion remained unchanged. The disturbances in electrolyte excretion were observed in full-term as well as in preterm neonates. Serum electrolyte levels remained unchanged. In conclusion, therapeutic doses of gentamicin result in urinary loss of sodium, calcium, and magnesium in neonates immediately after the infusion of the drug. These electrolyte changes may be of clinical importance, especially for sick preterm neonates.     

Case of cerebral salt wasting syndrome with difficulty in controling excessive urine volume

Symptoms of hyponatremia and diuresis due to cerebral salt wasting syndrome (CSWS) are often observed after aneurysmal subarachnoid hemorrhage (SAH). Inadequately treated CSWS is known to work as a trigger of symptomatic vasospasm in SAH patients. Therefore, it is indispensable to detect and treat CSWS as early as possible in ICU. A 36-year-old man with SAH was admitted to our ICU. His urine volume increased excessively 3 days after ICU admission, and it reached a peak (39,250 ml x day(-1)) on the 6th day in ICU. Since infusion volume was controlled with regard to daily urinary output, hyponatremia was not noticeable and excessive urine volume stood out conspicuously. Though vasopressin and desmopressin were administered, the symptoms of natriuresis and hyponatremia were aggravated, associated with hyper secretion of natriuretic peptides (ANP 160 pg x dl(-1), BNP 172 pg x dl(-1)). Recent studies revealed that hyponatremia and hypovolemia following SAH might be caused by exaggerated secretion of natriuretic peptides. Experimental studies showed that the administration of vasopressin and desmopressin cause excessive secretion of natriuretic peptides under the circumstance of volume expansion in rats. We infer that the administration of vasopressin and desmopressin to our patient deterionated natriuresis in CSWS as in the previous experimental findings.     

Effects of hydrochlorothiazide plus sotalol on acute urinary electrolyte excretion in normal subjects

Twenty-four-hour urinary outputs, total volume and urinary chlorine (Cl), sodium (Na), potassium (K), calcium, magnesium (Mg), total inorganic phosphate and creatinine levels were measured in 12 biologically equivalent healthy volunteers given single oral doses of placebo, hydrochlorothiazide (HCTZ) 50 mg and a combination of HCTZ and sotalol (STL) 320 mg in a double-blind, random study. HCTZ and HCTZ + STL increased urinary volume and Na, K, Cl, phosphate and Mg levels significantly and to a similar extent. Since HCTZ causes hyperkaliuresis and hypermagnesiuresis with or without simultaneous administration of STL, the latter does not change the acute effects of HCTZ in healthy subjects.     

Hyponatremia in neurologic intensive care: cerebral salt wasting syndrome and inappropriate antidiuretic hormone secretion

Hyponatraemia is a frequent complication in neurologically injured patients; it is a secondary cerebral injury. Hyponatraemia leads to consciousness problems, convulsions, worsening of the neurological status and thus the neurological evaluation. Hyponatraemia is secondary to free water retention (inappropriate ADH secretion) or to renal salt loss. The cerebral salt wasting syndrome (CSWS) has been described with head injury, subarachnoid haemorrhage and after several sorts of brain insults. It is characterised by an increased natriuresis and diuresis. Diagnosis is based on hyponatraemia, hypernatriuresis, increased diuresis and hypovolaemia. However, inappropriate ADH secretion and CSWS share several diagnostic criteria. The atrial natriuretic factor and the C-type natriuretic factors play a role in the development of the CSWS. The diagnostic approach and monitoring are based on the assessment of sodium and water losses. Therapy is based on correction of the circulating volume and natraemia. Speed of correction is a matter of debate: slow correction presents the risk of further neurological injury whereas rapid correction presents the risk of central pontine myelinosis.     

Elevated urinary C-peptide excretion in multiple trauma patients

A simple, indirect method of estimating integrated insulin secretion is the measurement of C-peptide, a byproduct of insulin biosynthesis, in plasma and in 24-hr urine samples. We determined, in 29 severely injured hypermetabolic and highly catabolic multiple trauma patients, the plasma level and daily excretion rate of C-peptide, 48-72 hrs postinjury. Data from a set of eight patients who underwent glucose-based total parenteral feeding for 6 days were analyzed for the course of changes in the excretory pattern of C-peptide and catecholamines. The molar ratio of plasma C-peptide to insulin in the trauma patients was similar to that in unstressed controls, indicating that the rate of hepatic insulin extraction is not appreciably altered due to trauma. This is also evident from a significant correlation (p = 0.001) between the plasma C-peptide and insulin levels. The excretion of C-peptide was elevated to three times the normal both in absolute terms and when normalized to creatinine excretion. This was also accompanied by a twofold increase in the plasma levels, indicating an enhanced secretion rate of C-peptide and hence of insulin in response to trauma. Injury-induced insulin resistance does not seem to be due to a decreased insulin secretion. An increase in insulin output would appear to be a significant and desirable response for a continued anabolic stimulus coexistent with the net catabolic phase. Parenteral feeding augmented the excretion of C-peptide and catecholamines and this effect peaked on the fourth day of nutritional therapy.     

Determinants of urinary nitrogen excretion in burned patients

A retrospective study of urinary urea excretion has been performed in 91 burned patients. Maximum mean excretion occurred between days 5 and 8 after injury. The rate of excretion during this peak period correlated significantly with the sex and age of the patient as well as the burn size. It is suggested that peak nitrogen excretion may be more accurately predicted if all three variables are considered. However, the wide variation seen in patient response and differences in clinical management mean that regular measurement of urinary urea excretion still provides the most reliable guide to dietary protein requirements after a burn.     

A simple index to estimate the likelihood of bacterial infection in patients developing fever after abdominal surgery

To identify predictors of bacterial infection in patients developing postoperative fever, we prospectively studied 434 adults who underwent abdominal surgery. Of the 434 study patients, 163 (38%) developed postoperative fever (38.1 degrees C [100.6 degrees F] or greater) and 26 (16%) of the febrile patients were found to have bacterial infection. Logistic-regression analysis showed that postoperative infection was associated with a WBC count of less than 5000 or greater than 10,000/mm3, a BUN of 15 mg/dl or greater, and fever onset after the second postoperative day. A predictive index, constructed from these three features, created a useful gradient for estimating the likelihood of postoperative infection. In patients with zero, one, two or three of the index features, the proportions having infection were 2 per cent (1/50), 14 per cent (12/88), 45 per cent (10/22), and 100 per cent (3/3), respectively (P less than 0.0001). This simple index, which uses readily available clinical data, may help reduce the cost of postoperative care by identifying patients with a low probability of infection in whom cultures, imaging studies, and empirical antibiotics do not appear necessary. Thorough diagnostic evaluation in patients with two or more index features may also reduce delay in the detection and treatment of postoperative infection. The predictive value of this index should be validated in a new patient set, however, before widespread application of the index is warranted.     

Increased urinary excretion of interleukin-17 in nephrotic patients

BACKGROUND/AIM: Interleukin (IL)-17 is a newly discovered cytokine that is secreted by activated memory CD4+ T cells and modulated the early stage of immune response. To elucidate the pathophysiology of minimal-change nephrotic syndrome (MCNS), we focused on IL-17, which is one of the key factors in regulating an inflammatory response, and thus determined the daily excretion of IL-17 in urine. METHODS: For this purpose, excretion levels of IL-17 were measured in the urine of patients with MCNS during relapse and remission using a highly sensitive sandwich enzyme-linked immunosorbent assay. The data obtained were compared with levels of daily urinary excretion of IL-17 in patients with IgA nephropathy (IgAN). A group of healthy subjects served as control. In both experimental groups urine levels of IL-17 excretion were plotted against their daily urinary protein excretion. RESULTS: We demonstrated increased levels of IL-17 excretion in the urine of patients with MCNS and IgAN as compared to the non-nephrotic and healthy controls. In MCNS the daily urinary IL-17 (uIL-17) excretion was increased and returned to baseline with remission of the nephrotic syndrome (NS). We also demonstrated a positive correlation between urinary protein excretion and daily uIL-17 excretion. CONCLUSION: Taken together, these data indicate that uIL-17 excretion is increased during the NS, suggesting the possibility that daily uIL-17 excretion may reflect the disease activity of NS.     

Enhanced urinary adiponectin excretion in IgA-nephropathy patients with proteinuria

Adiponectin is secreted specifically by adipose tissue. It was reported that the serum adiponectin level was markedly increased in patients with end-stage renal disease and was positively associated with abnormal renal function in type 2 diabetes. Recently, we found that urinary adiponectin level was significantly increased in type 2 diabetic patients with overt diabetic nephropathy, but not in those without nephropathy. The aim of the present study was to evaluate whether the urinary adiponectin level is increased not only in diabetic patients with macroalbuminuria but also in IgA-nephropathy patients with macroalbuminuria. We measured urinary adiponectin levels in 24 healthy control subjects, 12 IgA-nephropathy patients, and 19 type 2 diabetic nephropathy patients, and they were, in medians, 2.24 microg/g creatinine (ranges of 0.85 to approximately 3.70), 59.2 microg/g creatinine (4.95 to approximately 186), and 33.1 microg/g creatinine (4.69 to approximately 114), respectively. In the two patient groups, urinary adiponectin levels were significantly higher than in control subjects (P<0.01). Moreover, positive correlations between urinary adiponectin levels and albumin-to-creatinine ratios were observed in IgA-nephropathy (R2=0.53, P<0.01) and diabetic nephropathy patients (R2=0.61, P<0.01), but not in control subjects. Serum adiponectin levels were unchanged in these three groups. These findings suggested that the increase of urinary adiponectin levels partly results from enhanced filtration of circulating adiponectin through the changes of glomerular permselectivity and intraglomerular hydruric pressure. However, clinical implication of urinary adiponectin excretion in healthy control remains to be elucidated.