[Abolition of the natriuretic response to an acute water and sodium overload by indomethacin in dogs (proceedings)].
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Animals↗
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Sodium overload from Karo syrup.
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Humans↗
Sodium overload from Karo syrup.
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Body Weight↗
The effect of water, sodium overloading and diuretics upon urinary kallikrein.
The effects of acute administration of either water or 2% NaCl solution via a stomach tube and injections of diurecits, furosemide (5, 10 mg) and acetazoleamide (5, 20 mg per rat), in adult rats upon urinary kallikrein (Kal), Na and K, were studied. Hyperhydration with water (5% b.w.) produced in 121% increase and 2% NaCl overloading (5% b.w.) 275% increase in urinary Kal within 120 min after gavage, when compared with the excretion of non hyperhydrated rats. Furosemide 5 mg in hyperhydrated animals produced in the same period an excretion of 645 +/- 52 ng BR of Kal, which is 147% higher to that excreted by the hyperhydrated controls. The same dose of furosemide in 2% NaCl loaded rats, produced an excretion of Kal equivalent to 1333 +/- 72 ng BR which is 180% greater than in controls similarly loaded. Acetazoleamide 20 mg and furosemide 5 mg produced similar excretions of Kal even though natriuresis is greater tna kalliuresis is lesser in furosemide injected rats. Evaluation of total kidney Kal has shown that a single (10 mg) or a series of furosemide injections (8 days 5 mg + 1 day 10 mg), brings about a significant (p is less than 0.001) decrease in renal Kal, but the increase of Kal excreted in the urine (120 min) is 3.5 times more (under a single injection) and 42 times more (under 9 injections) than the amount which disappears from the kidneys. Apparently furosemide not only stimulates Kal excretion, but also Kal synthesis in the kidney. The results support the concept that the Kal system would be involved in excretory functions dealing both with sodium and water excretion.
Acetazolamide↗
Sodium Overload-Related Molecular Subtypes and a Four-Gene Prognostic Signature Predict Survival, Immune Landscape, and Therapeutic Response in Acute Myeloid Leukemia.
Sodium overload has recently emerged as a critical metabolic stressor involved in cancer progression; however, its molecular characteristics and clinical relevance in acute myeloid leukemia (AML) remain unexplored. RNA-seq data sets, clinical annotations, and mutational profiles of AML patients were annotations from The Cancer Genome Atlas and integrated with Genotype-Tissue Expression normal samples. Sodium overload-related genes (SORGs) were obtained from GeneCards. Differentially expressed SORGs (DESORGs) screened by applying the limma statistical model, followed by univariate Cox proportional hazards regression, consensus clustering, functional enrichment, immune infiltration analysis, and pathway evaluation. A prognostic signature was developed through least absolute shrinkage and selection operator regression followed by multivariate Cox modeling. The model's performance was further verified in two external GEO data sets (GSE71014 and GSE37642). Nomogram construction, subgroup analysis, tumor mutational burden (TMB) assessment, drug sensitivity prediction, transcription factor (TF) analysis, and competing endogenous RNA (ceRNA) network analyses were also performed. A total of 57 DESORGs were identified, and 2 sodium overload-related molecular subtypes exhibited distinct survival, immune infiltration, and inflammatory pathway activation. A robust four-gene signature (DOCK1, GABRE, HTR7, ACSM1) stratified patients into high- and low-risk categories with significantly different survival across training and validation cohorts. High-risk patients displayed increased immune infiltration, higher TMB, reduced sensitivity to multiple chemotherapeutic drugs, and inferior predicted response to PD-L1 blockade. TF and ceRNA networks revealed multilayered transcriptional and post-transcriptional regulation of the signature genes. This study identifies sodium overload-related molecular heterogeneity in AML and establishes a validated four-gene prognostic signature that integrates genomic, immunologic, and therapeutic features, offering potential utility for personalized risk assessment and treatment optimization.
Humans↗
[Degree of granularity of the atrial cardiocytes. Morphometric study in rats subjected to different types of water and sodium load (author's transl)].
Morphometric analysis was applied to the evaluation of the atrial cardiocytes specific granules, in rats subjected to different types of water and sodium load. In control animals, the right atrium is more granulated than the left one and the interauricular septum. Ipsilateral atrium and auricle have the same index of granularity. Five types of water and sodium load were tested - I. Full water restriction - II. Sodium restriction with normal water intake - III. Controls - IV. Sodium overloading - V. Sodium and Doca overloading. From groups I to V, the index of granularity decreases progressively. The same phenomenon does not appear in the left atrium, except for the group II (sodium restriction) whose index is higher (p less than 0.001) than in the other groups. These data are not incompatible with the existence of a relationship between the presence of atrial specific granules and the atrial volosensitivity. An analogy between these cells and the myopithelioid cells of the juxtaglomerular apparatus is then suggested.
Animals↗
[Physiopathology of arterial hypertension in chronic hemodialysis patients].
The increase in total body sodium and hyperactivity of the renin-angiotensin system plays a major part in hypertension in patients underdoing chronic dialysis. After sodium depletion most patients become normotensive. Their hypertension seems to be due to sodium overload but it is favoured by insufficient inhibition of renin secretion. Some renin hypertensive, hypersecretion of renin is the main factor in these cases but its effect is aggravated by the sodium overload. Other factors may play a role as suggested by the studies of hypertensive patients after bilateral nephrectomy. However, their roles and mechanisms are unknown at present.
Humans↗
Construction of molecular signatures based on the co-expression network of NECSO-related gene TRPM4 and its prognostic value in hepatocellular carcinoma.
BACKGROUND: Hepatocellular carcinoma (HCC) demonstrates significant prognostic variability that is not entirely accounted for by traditional staging systems. Necrosis by sodium overload (NECSO) is an emerging programmed cell death pathway, but its clinical relevance in HCC remains undefined. Therefore, this study aimed to identify TRPM4-associated core genes, develop and validate a prognostic signature, and investigate its relationship with the tumor immune microenvironment, tumor mutational burden, and single-cell expression patterns in HCC. METHODS: We integrated transcriptomic, clinical, and mutational datasets from The Cancer Genome Atlas-Liver Hepatocellular Carcinoma (TCGA-LIHC) (n=421) and Gene Expression Omnibus (GEO) cohorts (n=115) to identify genes co-expressed with TRPM4-a key NECSO mediator-and those differentially expressed in HCC. A prognostic signature was developed using least absolute shrinkage and selection operator (LASSO)-Cox regression and validated through survival analysis, time-dependent receiver operating characteristic (ROC) curves, and multivariate Cox regression analysis. The immune landscape was characterized using CIBERSORT, somatic mutation data were used to calculate tumor mutational burden (TMB) and assess its correlation with the risk score, and single-cell RNA sequencing (scRNA-seq) resolved cell-type-specific expression patterns. RESULTS: From 294 TRPM4-associated core genes, we identified an 11-gene signature (BRSK1, MMP1, GRIN2D, GP6, MYOM2, N4BP3, CCDC112, TSEN54, MAP3K9, SPP1, B3GNT4) that independently predicted overall survival (OS) (hazard ratio =5.419, P<0.001) with areas under the curve (AUCs) of 0.779, 0.693, and 0.701 at 1, 3, and 5 years. These values were superior or comparable to conventional clinicopathologic variables after direct comparison. High-risk patients exhibited an immunosuppressive microenvironment, characterized by enrichment of M0 macrophage, a higher M2/M1 ratio (P<0.001) and distinct immune checkpoint profiles. When integrated with TMB, the prognostic stratification was further refined: high-TMB/high-risk patients had poorest outcomes (median OS, 15.3 months), while low-TMB/low-risk patients had the most favorable survival (median OS, 68.7 months). Single-cell analysis revealed that MMP1 was induced in cancer-associated fibroblasts (CAFs) and SPP1 was downregulated in macrophages, single-cell risk scores confirmed TAFs and macrophages as the main contributors to the prognostic model. CONCLUSIONS: The TRPM4-centered 11-gene signature provides robust and independent prognostic stratification in HCC by integrating immune, mutational, and single-cell features. This signature serves as a potential tool for prognostic evaluation and may help inform immunotherapeutic strategies for HCC.
Hepatocellular carcinoma (HCC)↗
[Severe hyperkalemia in cardiac patients].
Hyperkalaemia with severe myocardial consequence may complicate the treatment of heart failure. In five patients who developed kalaemia ranging from 6.5. to 8.6. mEq/l, the ECG showed altered auriculogram and/or widened QRS, the latter change being associated with ST segment elevation and very large T wave in one case. Such hyperkalaemia cannot be termed iatrogenic, although it is promoted by diuretic-induced hyponatraemia and dehydration. The essential part is played by an aggravation of the haemodynamic status, responsible for acute renal insufficiency with oligoanuria, and by the attendant metabolic acidosis. The correction of this metabolic acidosis promotes diuresis, causing potassium depletion and the rapid regression of electrocardiographic abnormalities. Parenteral alkalinization with sodium bicarbonate, associated with furosemid to prevent sodium overload, instituted in emergency, is the only way to prevent asystole or ventricular fibrillation when kalaemia exceeds 8 mEq/l.
Acidosis↗
An investigation into the pathogenesis of hypertension in acromegaly.
1. In 29 patients with acromegaly, plasma renin activity and growth hormone were measured during fasting and recumbency on free diet. Exchangeable sodium was measured in all cases and expressed as a percentage of the expected value on the basis of lean body mass. 2. Twenty-two control subjects without evidence of cardiovascular, renal or endocrine disease were studied in the same way. 3. There was a significant increase in exchangeable sodium and suppression of plasma renin activity in the acromegalic patients in comparison with control subjects. 4. There was a significant positive correlation between exchangeable sodium and plasma growth hormone. 5. Hypertensive acromegalic patients (diastolic blood pressure larger than or equal to 100 mmHg) tend to have a lower (although not significantly so) exchangeable sodium than normotensive subjects. 6. We conclude that (a) suppression of plasma renin activity in acromegaly can be explained by sodium retention, (b) hypersecretion of growth hormone is probably responsible for the increased exchangeable sodium, and (c) sodium overload cannot be directly related to blood pressure but may contribute to the increased occurrence of hypertension in acromegaly.
Acromegaly↗
The use of saralasin in the recognition of angiotensinogenic hypertension.
Specific antagonists of angiotensin II (AII) such as saralasin might theoretically be of great value in the recognition of angiotensinogenic hypertension. Evidence is presented to show the importance of overcoming any existing sodium overload and of administering saralasin first in small and then in larger amounts by infusion (or injection). When this was done in 600 hypertensive patients, 62 showed a fall in blood pressure of more than 10/8 mm Hg. Further tests in 50 of these subjects indicated that the fall in blood pressure was associated with high peripheral levels of plasma renin activity (PRA) and/or abnormal renal vein PRA ratios in 94%. The procedure rarely failed to detect even mild forms of angiotensinogenic hypertension. In 62 patients found to have angiotensinogenic hypertension, the responsible lesions included unilateral renal arterial stenosis with good contralateral renal function (29%), bilateral renal disease (21%), Cushing's syndrome (6%), small vessel disease or specific excess of renin production - without other detectable renal disease - (31%) and incompletely evaluated disorders (13%). Saralasin has been of great value in simply and reliably demonstrating the presence or absence of an angiotensinogenic component in a large group of hypertensive patients.
Adult↗
Importance of the plasma refilling rate in the genesis of hypovolaemic hypotension during regular dialysis and controlled sequential ultrafiltration-haemodialysis.
The effects of ultrafiltration (UF) on plasma volume (PV) have been studied in eight patients using regular dialysis (RD) and controlled sequential ultrafiltration-haemodialysis (CSU) performed with a Rhodial 75 dialysis system. For a given value of UF the reduction of PV is determined by the plasma refilling rate. During CSU ultrafiltration induces a rapid increase in oncotic pressure without decreasing plasma osmolality. The high plasma refilling rate which can reach 1500 ml/hr allows moderate hypovolaemia despite high rates of UF and contributes to the usual good clinical tolerance of CSU. During RD a rapid decrease in plasma osmolality contributes to a water shift from the vascular space towards the interstitial and intracellular spaces and severe hypovolaemia can occur despite moderate ultrafiltration. CSU offers an adequate treatment for sodium overloaded patients with hypervolaemia, but is of no benefit in routine conditions.
Humans↗
Acute pulmonary edema after the intravenous administration of contrast media.
Acute pulmonary edema developed in two young, previously healthy women immediately after the intravenous administration of contrast media. The pulmonary edema, rare in young persons, could not be explained by classical anaphylaxis, contrast media overdose, sodium and fluid overload, or acute myocardial infarction. A nonimmunologic osmotic mechanism causing reversible pulmonary capillary leak might explain the clinical events observed in both patients. Both responded to continuous positive airway pressure (CPAP), indicating the possible utility of CPAP in treating pulmonary capillary-leak contrast reactions.
Adolescent↗
Nephrotic syndrome: vasoconstriction and hypervolemic types indicated by renin-sodium profiling.
Studies of 16 adults with nephrotic edema reveal a spectrum of disease, the extremes of which suggest two different pathophysiologic forms. Patients with the "classic" form--vasoconstriction or hypovolemic nephrosis--have high renin and aldosterone levels that are stimulated rather than suppressed by salt-loading but become lower before steroid diuresis. These patients have minimal lesion disease and, perhaps from diffuse capillary damage, tend to have hypovolemia with renin-induced vasoconstriction. Patients with the second, and heretofore undescribed, form--hypervolemic or overfilling nephrosis--have low renin and aldosterone values that rise normally after sodium depletion. Hypertension, mild renal insufficiency, hypervolemia, and steroid resistance with chronic glomerulonephritis are seen histologically. This form appears volume overloaded from impaired renal sodium excretion. In remission of either type, renin system deviations tend towards normal, but one form does not convert to the other. Renin-sodium profiling may help reveal the two forms and predict steroid responsiveness.
Adolescent↗
Synthesis and evaluation of the thiosemicarbazone, dithiocarbazonate, and 2'-pyrazinylhydrazone of pyrazinecarboxaldehyde as agents for the treatment of iron overload.
Three prototype tridentate ligands (i.e., pyrazinecarboxaldehyde thiosemicarbazone, sodium pyrazinecarboxaldehyde dithiocarbazonate, and pyrazinecarboxaldehyde 2'-pyrazinylhydrazone) were prepared and evaluated for their relative abilities to remove iron from model systems designed to mimic particular aspects of chronic transfusional iron overload. These compounds were synthesized by condensation of pyrazinecarboxaldehyde with the appropriate substituted hydrazide. Iron-binding properties were determined, and the ability to remove iron from the proteins transferrin and ferritin was ascertained. An in vivo model system employing iron-loaded mice was used to demonstrate that all three compounds were effective at reducing tissue iron levels.
Animals↗
[Haemodialysis in the treatment of biguanide-induced lactate acidosis (author's transl)].
Severe lactate acidosis developed in nine diabetics on biguanide. When lactate acidosis was diagnosed all patients had reduced renal function, six being oligoanuric. Pre-existing chronic renal failure as a factor in the development of lactic acidosis was excluded in five patients, normal renal function being restored later. All patients were dialysed, seven surviving. This mortality rate is lower than that reported by others for biguanide-induced lactate acidosis. Rapid biguanide elimination by dialysis was demonstrated both in vitro and in vivo. The in vivo clearance of buformin was 83 +/- 43 ml/min (mean +/- SD, n = 4), that of phenformin 68 +/- 33 ml/min (n = 7). The main advantages of haemodialysis in the treatment of biguanide-induced lactic acidosis are rapid removal of toxic biguanides and excess lactate and the ability to administer sodium bicarbonate adequately without risking hypernatraemia and fluid overload.
Acidosis↗
[Latent renal tubular acidosis of the cirrhotic patient. Study of urinary excretion of protons and sodium].
Patients suffering from hepatic cirrhosis develop renal tubular acidosis when subjected to an acid overload. This is characterised by a fall in plasma pH and bicarbonate and by inability of the kidney to lower urine pH and to excrete a sufficient quantity of protons in the form of titratable acidy and ammonia. This disturbance is difficult to explain. It may form part of the picture of the classical functional renal insufficiency of the cirrhotic and may be a particular result of altered renal haemodynamics. Detected by the acidification test, this abnormality may be demonstrated in the absence of any other involvement of renal function. The severity of this renal tubular acidosis would appear to be related to the degree of hepatic disease.
Acidosis, Renal Tubular↗
Bicarbonate-buffered peritoneal dialysis. An effective adjunct in the treatment of lactic acidosis.
Severe lactic acidosis is associated with poor prognosis. Usually, the patient is treated with massive amounts of intravenous sodium bicarbonate, which in itself carries many undesirable consequences such as fluid overload and hypernatremia. We have successfully used peritoneal dialysis with a bicarbonate-buffered dialysate in the management of severe acidosis. Bicarbonate-buffered peritoneal dialysis provided an unlimited supply of physiologic buffer over a prolonged period without causing hypervolemia or hypernatremia. Furthermore, significant amounts of lactate were removed by dialysis. We, therefore, recommend the use of bicarbonate-buffered peritoneal dialysis as an adjunct in the treatment of severe lactic acidosis.
Acidosis↗