Divalent Ion Excretion in Chronic Kidney Disease: Relation to Degree of Renal Insufficiency

1970 ◽  
Vol 38 (3) ◽  
pp. 297-307 ◽  
Author(s):  
M. M. Popovtzer ◽  
L. I. Schainuck ◽  
S. G. Massry ◽  
C. R. Kleeman
Keyword(s):  
Renal Failure ◽  
Renal Insufficiency ◽  
Renal Disease ◽  
Close Association ◽  
Fractional Excretion ◽  
Normal Subjects ◽  
Common Mechanism ◽  
Severe Renal Failure ◽  
Renal Handling ◽  
Sodium Magnesium

1. The excretory patterns of sodium, calcium, magnesium and phosphorus were evaluated in seventy-eight patients with varying degrees of renal insufficiency, and in twelve normal subjects. 2. In mild renal failure the fractional excretion of filtered sodium, magnesium and phosphorus are significantly higher while that of calcium is significantly lower than values seen in normals. In advanced renal failure the fractional excretions of the filtered loads of all these ions increase steeply. These patterns are not influenced by the type of renal disease. 3. The fractional excretions of filtered sodium and calcium, calcium and magnesium, and sodium and magnesium were plotted against each other. The analysis of the plots showed that the fractional excretions of their filtered loads correlate poorly in patients with mild and moderate renal insufficiency, but closely in patients with severe renal failure. 4. These results indicate that the relation between the renal handling of divalent ions is not uniform at all levels of renal insufficiency. The dissociation between the excretory patterns observed in patients with early renal failure is consistent with the concept that different mechanisms may influence each individual ion separately. This is in contrast to the close association which exists between the excretory patterns of these ions in patients with advanced renal disease, and in which a single common mechanism may underlie the renal handling of these ions.

Functional adaptation to reduction in renal mass

1979 ◽  
Vol 59 (1) ◽  
pp. 137-164 ◽  
Author(s):  
J. P. Hayslett
Keyword(s):  
Renal Failure ◽  
Renal Function ◽  
Renal Insufficiency ◽  
Renal Disease ◽  
Tubular Reabsorption ◽  
Functional Adaptation ◽  
Severe Renal Failure ◽  
Nephron Segments ◽  
Endogenous Production ◽  
Severe Renal Insufficiency

As the population of nephrons diminishes, while the dietary intake and/or endogenous production of water and solutes is unchanged, there is a proportional increase in the excretion of water and solute by individual residual nephrons. This adaptive change, which preserves zero net balance in the early phase of renal insufficiency, involves a reduction in the fractional reabsorption of substances derived from the initial glomerular ultrafiltrate and an increase in the rate of secretion of solutes that are extracted by tubular epithelial cells from peritubular blood. These compensatory changes are adequate to maintain electrolyte and water homeostasis until severe renal failure ensures (GFR less than 20% of normal). After a moderate reduction in nephron population there is no evidence that the factors that modulate ion transport are qualitatively different from those that regulate renal function in the intact subject, when the excretory load of solute is varied by changes in intake or endogenous production. In severe renal insufficiency, however, it seems likely that several factors, not present in the subject with intact renal function, also play an important role in modifying the excretion of water and electrolytes. For example, an osmotic diuresis in severe renal failure apparently decreases the tubular reabsorption of sodium and divalent cations and that of water. Moreover, elaboration of a partially identified "natriuretic" substance may participate in the regulation of electrolyte excretion in severe renal insufficiency. The appearance of these factors in severe renal insufficiency probably complements mechanisms that normally regulate the transfer of water and ions across tubular epithelium, since even after a marked reduction in GFR the urinary excretion of solutes and water changes proportionally with intake, although within narrower limits than exist in normal subjects. Studies in experimental animals and in man with acquired renal disease demonstrate the important role of other factors in compensatory adaptation, in addition to changes in tubular transport. The marked increases in glomerular filtration rate and nephron blood flow, which occur at least in some conditions, increase the absolute amount of water and solute delivered to the various nephron segments in ultrafiltrate and peritubular blood. Moreover, the expansion of extracellular fluid in severe renal failure inhibits tubular reabsorption of filtered water and solute in the same qualitative way that has been demonstrated in subjects with intact renal function. Quantitatively the response to acute volume expansion is exaggerated compared with control. Concomitant changes in renal hypertrophy and hyperplasia probably play an important role in functional adaptation. The apparent marked capacity for compensatory growth in all nephron segments and even in portions of tubular segments in parenchymal renal disease increases the area for transport by tubular epithelia in residual nephrons, as the overall number of nephrons diminishes...

A Study on the Distribution of Body Fluids after Rapid Saline Expansion in Normal Subjects and in Patients with Renal Insufficiency: Preferential Intravascular Deposition in Renal Failure

1983 ◽  
Vol 64 (2) ◽  
pp. 153-160 ◽  
Author(s):  
Hendrik A. Koomans ◽  
Anton B. Geers ◽  
Peter Boer ◽  
Jan C. Roos ◽  
Evert J. Dorhout Mees
Keyword(s):  
Renal Failure ◽  
Blood Volume ◽  
Plasma Volume ◽  
Extracellular Fluid ◽  
Normal Subjects ◽  
Distribution Volume ◽  
Fluid Distribution ◽  
Severe Renal Failure ◽  
Control Value ◽  
Stage Renal Disease

1. The effect of rapid intravenous infusion of 25 ml of isotonic sodium chloride solution (saline)/kg body weight on extracellular fluid volume (ECFV, 82Br distribution volume), plasma volume (131I-labelled albumin distribution volume) and blood volume (from plasma volume and packed cell volume) was studied in nine normal subjects and a group of 11 patients with end-stage renal disease (ESRD). 2. Immediately after the infusion, the increases in ECFV were equal in the two groups but the increases in plasma and blood volumes were significantly larger in the patients with ESRD. .3. Ninety minutes after the end of the infusion, the blood volume/ECFV ratio was significantly decreased from the control value in the normal subjects, but slightly increased in the patients with ESRD. 4. It is concluded that in severe renal failure the control of fluid distribution is changed in a way which leads to a preferential distribution of rapidly infused saline into the intravascular compartment.

Hepatic Metabolism of Aminopyrine in Patients with Chronic Renal Failure

1978 ◽  
Vol 54 (2) ◽  
pp. 133-140 ◽  
Author(s):  
S. Scherrer ◽  
B. Haldimann ◽  
A. Küpfer ◽  
F. Reubi ◽  
J. Bircher
Keyword(s):  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Insufficiency ◽  
Serum Creatinine ◽  
Hepatic Metabolism ◽  
Normal Subjects ◽  
Hepatic Disease ◽  
Dialysis Treatment ◽  
History Of ◽  
Aminopyrine Demethylation

1. To evaluate potential alterations in hepatic metabolism of drugs occurring in patients with renal insufficiency the fate of aminopyrine was studied in 17 patients with chronic renal failure and in 27 normal subjects. 2. Although patients with chronic renal failure exhibited large variations, their aminopyrine plasma disappearance times (mean 0·62 ± sd 0·24 h−1) were significantly higher than those found in normal subjects (0·30 ± 0·07 h−1, P < 0·002). 3. 14CO2 derived from [dimethylamine-14C]aminopyrine disappeared from breath more rapidly in patients with chronic renal failure and a history of analgesic abuse (0·40 ± 0·04 h−1) than in control subjects (0·22 ± 0·03 h−1, P < 0·01) and in other patients with chronic renal failure (0·24 ± 0·04 h−1). 4. Dialysis treatment and serum creatinine concentrations were not correlated with the rates of aminopyrine metabolism. Two additional patients, however, with combined renal and hepatic disease, exhibited markedly slowed rates of aminopyrine demethylation. 5. Although chronic renal failure by itself might not alter microsomal drug metabolism it is concluded that, in patients with a history of abuse of phenacetin-containing analgesics, marked acceleration in aminopyrine N-demethylation may be observed.

scholarly journals Evidence for net renal tubule oxalate secretion in patients with calcium kidney stones

2011 ◽  
Vol 300 (2) ◽  
pp. F311-F318 ◽  
Author(s):  
Kristin J. Bergsland ◽  
Anna L. Zisman ◽  
John R. Asplin ◽  
Elaine M. Worcester ◽  
Fredric L. Coe
Keyword(s):  
Fractional Excretion ◽  
Normal Subjects ◽  
Tubular Secretion ◽  
Idiopathic Hypercalciuria ◽  
Renal Handling ◽  
Stone Formers ◽  
Oxalate Secretion ◽  
Calcium Phosphorus ◽  
Urine Oxalate ◽  
Urinary Oxalate Excretion

Little is known about the renal handling of oxalate in patients with idiopathic hypercalciuria (IH). To explore the role of tubular oxalate handling in IH and to evaluate whether differences exist between IH and normal controls, we studied 19 IH subjects, 8 normal subjects, and 2 bariatric stone formers (BSF) during a 1-day General Clinical Research Center protocol utilizing a low-oxalate diet. Urine and blood samples were collected at 30- to 60-min intervals while subjects were fasting and after they ate three meals providing known amounts of calcium, phosphorus, sodium, protein, oxalate, and calories. Plasma oxalate concentrations and oxalate-filtered loads were similar between patients (includes IH and BSF) and controls in both the fasting and fed states. Urinary oxalate excretion was significantly higher in patients vs. controls regardless of feeding state. Fractional excretion of oxalate (FEOx) was >1, suggesting tubular secretion of oxalate, in 6 of 19 IH and both BSF, compared with none of the controls ( P < 0.00001). Adjusted for water extraction along the nephron, urine oxalate rose more rapidly among patients than normal subjects with increases in plasma oxalate. Our findings identify tubular secretion of oxalate as a key mediator of hyperoxaluria in calcium stone formers, potentially as a means of maintaining plasma oxalate in a tight range.

scholarly journals Pathophysiological role and diuretic efficacy of atrial natriuretic peptide in renal patients.

1997 ◽  
Vol 8 (3) ◽  
pp. 445-455 ◽  
Author(s):  
L De Nicola ◽  
V Bellizzi ◽  
B Cianciaruso ◽  
R Minutolo ◽  
G Colucci ◽  
...  
Keyword(s):  
Fractional Excretion ◽  
Normal Subjects ◽  
Renal Perfusion ◽  
Renal Handling ◽  
Sodium Diet ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Pathophysiological Role ◽  
Dose Dependent ◽  
Significant Increment

It has been suggested that renal disease is characterized by the presence of resistance to the natriuretic effects of atrial peptide (ANP). In this study, plasma ANP (pANP) and renal function were evaluated during stepwise infusion of low ANP doses (2, 4, 8, and 16 ng/kg per min) in glomerulonephritic patients with (CRF) or without (GN) moderate renal failure, and in normal subjects (NOR), kept at low-sodium diet (LSD; 35 mEq NaCl/day). To assess the physiological ANP levels, pANP was also measured in the three groups after normal-sodium diet (NSD; 235 mEq NaCl/day). ANP did not affect systemic and renal perfusion at any of the doses tested; a significant increment of GFR was observed only in NOR and GN. The 2-, 4-, and 8-ng/kg doses increased pANP to values overlapping the physiological concentrations measured at NSD; this was associated with a dose-dependent increment of urinary excretion of sodium (UNaV) that reached analogous levels in the three groups. ANP accounted for approximately 40% of the UNaV increment evoked by NSD in patients and in normal subjects. The 16-ng/kg dose led to supraphysiological levels that induced a similar marked enhancement of UNaV (from the basal value of 0.12 +/- 0.02 to 0.42 +/- 0.08 mEq/min in CRF, from 0.13 +/- 0.02 to 0.73 +/- 0.08 in GN, and from 0.09 +/- 0.02 to 0.49 +/- 0.11 in NOR). In CRF, the normal natriuretic response to the highest dose was caused by a larger increase of fractional UNaV that was strictly dependent on the greater pANP increment, as demonstrated by similar changes in the fractional excretion of cGMP, and, in part, on the greater aldosterone decrease. In all groups, ANP also induced a dose-dependent urinary loss of phosphate, potassium, and urea, resulting in a significant 15 to 25% decrease in the plasma levels. Thus, in GN and CRF patients, ANP plays a significant role in the renal handling of sodium; moreover, the achievement of low supraphysiological pANP levels leads to a conspicuous natriuresis associated with unique extranatriuretic effects.

Urinary and Whole Blood Cadmium Concentrations in Renal Disease

1973 ◽  
Vol 10 (1-6) ◽  
pp. 107-110 ◽  
Author(s):  
Elizabeth G. Willden
Keyword(s):  
Renal Failure ◽  
Renal Disease ◽  
Whole Blood ◽  
Reliable Method ◽  
Normal Subjects ◽  
Smoking Habits ◽  
Renal Diseases ◽  
Blood Cadmium ◽  
Health And Disease

A reliable method for the determination of cadmium in blood has been developed, and the concentrations in normal subjects and in patients with various types of renal failure determined. Dependency on, and variation with, age, sex and smoking habits in both health and disease have been investigated. The correlation of cadmium concentrations with renal diseases and their progress is postulated.

scholarly journals Methamphetamine (N-methylamphetamine)-induced renal disease: underevaluated cause of end-stage renal disease (ESRD)

2019 ◽  
Vol 12 (9) ◽  
pp. e230288 ◽  
Author(s):  
Krishna M Baradhi ◽  
Samata Pathireddy ◽  
Subhasish Bose ◽  
Narothama Reddy Aeddula
Keyword(s):  
Renal Failure ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Healthcare Workers ◽  
Uncontrolled Hypertension ◽  
Severe Renal Failure ◽  
Crystal Meth ◽  
Public Health Professionals ◽  
Stage Renal Disease ◽  
End Stage

A 26-year-old Caucasian man with no medical history, except years of oral and intravenous drug abuse, presented with fatigue, shortness of breath, epistaxis and uncontrolled hypertension. He was pale with skin ecchymosis over his thighs and was anaemic, with severe renal failure and metabolic acidosis. Following initial clinical stabilisation of the patient, a renal biopsy was obtained, which showed vascular and glomerular changes consistent with thrombotic microangiopathic injury and advanced glomerulosclerosis. He was treated with antihypertensives and required haemodialysis. He admitted using ‘crystal meth’ regularly for many years, which is likely responsible for his renal failure. We present the case to illustrate methamphetamine-induced renal disease leading to end-stage renal disease and to bring awareness among practising clinicians, ancillary healthcare workers and public health professionals of this often undervalued cause of renal failure, which can be prevented.

Concentrations of atrial natriuretic peptide in plasma and urine of kidney disease patients

1990 ◽  
Vol 36 (9) ◽  
pp. 1650-1653 ◽  
Author(s):  
F Marumo ◽  
H Sakamoto ◽  
K Ando ◽  
T Ishigami ◽  
T Ishigama
Keyword(s):  
Atrial Natriuretic Peptide ◽  
Renal Disease ◽  
Natriuretic Peptide ◽  
Renal Mass ◽  
Fractional Excretion ◽  
Normal Subjects ◽  
Specific Radioimmunoassay ◽  
Highly Sensitive ◽  
Single Nephron ◽  
Atrial Natriuretic

Abstract Concentrations of human atrial natriuretic peptide-like immunoreactivity (hANP-LI) were measured by a highly sensitive and specific radioimmunoassay (Biochem Biophys Res Commun 1986;137:231-6) in normal subjects and in renal disease patients without accompanying congestive heart failure, hypertension, edema, diabetes, or pregnancy. We attempted to clarify whether the hANP-LI concentration in plasma was increased by loss of renal mass. We found no correlation between the hANP-LI concentration in plasma and creatinine clearance (Ccr, 4.6-122.3 mL/min) in patients with renal disease (n = 63, r = -0.196), nor between hANP-LI concentrations in plasma and urine (n = 97, r = -0.207). The fractional excretion of hANP (FEhANP) correlated significantly with Ccr (n = 63, r = 0.520, P less than 0.01) and with FENa (n = 35, r = -0.503, P less than 0.01). Increased FEhANP in patients with chronic renal failure may have resulted because of an increase in single-nephron glomerular filtration rate similar to the FENa increase in these patients. The present data indicate that decreased renal function itself does not increase the concentration of hANP-LI in plasma.

Accumulation of Sulphur-Containing Amino Acids Including Cysteine-Homocysteine in Patients on Maintenance Haemodialysis

1980 ◽  
Vol 58 (5) ◽  
pp. 427-430 ◽  
Author(s):  
D. E. L. Wilcken ◽  
Vatsala J. Gupta ◽  
S. G. Reddy
Keyword(s):  
Amino Acids ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Renal Insufficiency ◽  
Serum Creatinine ◽  
Normal Subjects ◽  
Chronic Haemodialysis ◽  
Maintenance Haemodialysis ◽  
Acidic Amino Acids ◽  
Rate Of Accumulation

1. Plasma sulphur-containing amino acids were measured in 19 patients with renal failure on chronic haemodialysis and in 22 normal subjects, to determine the rate of accumulation of these amino acids in chronic azotaemia. 2. Cysteine-homocysteine mixed disulphide was significantly increased in patients before dialysis and homocystine was detected in low concentration in 10 patients. Cystine and taurine were also increased. Changes in other neutral and acidic amino acids were similar to those reported in chronic renal insufficiency. 3. In 3–4 h of dialysis serum creatinine was decreased by a mean of 55%, cysteine-homocysteine by 41%and cystine by 58.5%(P<0.001 for each). Methionine concentrations were normal throughout. 4. We conclude that sulphur-containing amino acids, except methionine, accumulate in chronic renal failure as rapidly as creatinine.

Platelet Numbers and Life Span in Acute and Chronic Renal Failure

1967 ◽  
Vol 17 (03/04) ◽  
pp. 532-542 ◽  
Author(s):  
J. H Stewart
Keyword(s):  
Renal Failure ◽  
Blood Transfusion ◽  
Renal Disease ◽  
Life Span ◽  
Chronic Renal Disease ◽  
Renal Unit ◽  
Severe Renal Failure ◽  
Number Of Patients ◽  
Significant Difference ◽  
Previous Blood Transfusion

SummaryPlatelet numbers were estimated on all 225 patients admitted with severe renal failure to the Sydney Hospital Renal Unit in a 2 year period. Serial counts were per formed to determine the circumstances under which platelet numbers were restored to normal in patients with thrombocytopenia. Measurements of 51Cr-labelled autologous or homologous platelet life span were made in 37 patients with severe renal disease and in 8 control subjects.Thrombocytopenia occurred in one quarter of all patients with renal tubular necrosis, acute or subacute glomerulonephritis, or malignant hypertension, but only in one twelfth of those with severe uraemia due to chronic renal disease. Recovery of platelet numbers followed partial relief of uraemia by dialysis or return of renal function in 24 patients. In 2 patients the platelet count rose despite no relief of uraemia, and in 14, there was no recovery from thrombocytopenia before death. Severe infection, microangiopathy and malignant disease, although present in a number of patients, were not important causes of thrombocytopenia.The life span of autologous platelets, or of compatible, normal, homologous platelets given to subjects who had never received a previous blood transfusion, was normal in severe renal failure, and there was no significant difference between patients with various types or different severities of renal disease. The survival of homologous platelets was slightly or moderately reduced when given to patients who had received a previous blood transfusion.The mean recovery of autologous 51Cr-labelled platelets prepared in acid citrate was 58%, and of homologous platelets, 41 %.Thrombocytopenia in renal failure is presumed to be mainly due to impaired platelet production caused by the biochemical affects of azotaemia. The condition should be treated by peritoneal dialysis, and, when this is impossible or ineffective, by platelet transfusion.

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