Functional Impairment in Chronic Renal Disease

Gonick, Harvey C.; Maxwell, M.H.; Rubini, Milton E.; Kleeman, C.R.

doi:10.1159/000179471

Cited by 24 publications

(2 citation statements)

References 10 publications

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“…In the presence of relative aldosterone refractoriness, higher doses of mineralocorticoids may be effective—for instance, in the case of Daughaday and Rendleman (32) in which the increase of the dose of substitutive mineralocorticoid abolished hyperkalemia. We have used much higher doses of mineralocorticoid than have previous authors (1, 3, 23). Thus, in our case, the refractoriness to aldosterone was practically absolute.…”

Section: Discussionmentioning

confidence: 58%

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Hyperkalemia and Coma Associated with Renal Tubular Acidosis in an Old Patient with Refractory Edema Due to the Nephrotic Syndrome: Furosemide‐Bicarbonate Therapy

Szende¹,

J²,

Takó³

et al. 1972

J American Geriatrics Society

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In a 70‐year‐old man, renal tubular acidosis and hyperkalemia occurred together with the nephrotic syndrome and stable chronic renal failure associated with diuretic‐refractory edema. Apparently an extreme medullary hyaline sclerosis accompanying nephroarteriosclerosis was the anatomical basis of the insufficiency of distal potassium and hydrogen‐ion secretion. The patient was refractory even to excessive doses of exogenous aldosterone. Therefore the edema was attributed exclusively to an increase of proximal tubular sodium reabsorption. The renal tubular acidosis was predominantly of the distal type, but the high daily bicarbonate requirement indicated also the presence of a proximal component. Hyperkalemia presumably was caused by the lack of aldosterone effect, but excessive proximal tubular sodium reabsorption also may have played a part. With or without the influence of diuretics, a definite correlation could be demonstrated between the osmolal clearance and the potassium clearance. The decrease of hyperkalemia caused by furosemide, ethacrynic acid and hydrochlorothiazide was attributed to an enhanced sodium‐for‐potassium exchange in the distal tubules due to the increased sodium load induced by these drugs. The “refractory edema” could be drained off by high doses of furosemide (1600 mg a day) even in the presence of progressive impairment of renal function. By the intravenous infusion of high doses of furosemide and bicarbonate, the acidotic and hyperkalemic coma of this patient with “refractory edema” was successfully combatted several times.

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Section: Discussionmentioning

confidence: 58%

“…Acid loading was carried out by the method of Wrong and Davies (22) as modified slightly by Gonick et al (23). The plasma Cortisol level was estimated according to Mattingly's method (24).…”

Section: Methodsmentioning

confidence: 99%

Hyperkalemia and Coma Associated with Renal Tubular Acidosis in an Old Patient with Refractory Edema Due to the Nephrotic Syndrome: Furosemide‐Bicarbonate Therapy

Szende¹,

J²,

Takó³

et al. 1972

J American Geriatrics Society

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Polycystic Disease and Hepatic Fibrosis in Children

Anand¹

1975

Am J Dis Child

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Renal function studies were done in five children with infantile polycystic disease (IPCD)of kidneys and liver and in four with congenital hepatic fibrosis (CHF). Glomerular filtration rate was reduced in all IPCD patients and in two of four CHF patients. Urinary concentrating ability following water deprivation and vasopressin administration was impaired in all IPCD patients and in three of four CHF patients. During control period, all patients had asymptomatic metabolic acidosis with total carbon dioxide content less than or equal to 20.5 millimols/liter, and net acid excretion (NAE) was reduced in all but one. Ammonium chloride was administered to seven patients; NAE increased in all, but the increments were subnormal in four. The inability to excrete maximally concentrated urine and an adequate amount of net acid may best be explained by abnormal tubular structure or alterations in medullary architecture secondary to progressive scarring, or both.

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Urologic Aspects of Renal Hypertension

Ziegler¹,

Mast²

1982

Arterial Hypertension

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Functional Impairment in Chronic Renal Disease

Cited by 24 publications

References 10 publications

Hyperkalemia and Coma Associated with Renal Tubular Acidosis in an Old Patient with Refractory Edema Due to the Nephrotic Syndrome: Furosemide‐Bicarbonate Therapy

Hyperkalemia and Coma Associated with Renal Tubular Acidosis in an Old Patient with Refractory Edema Due to the Nephrotic Syndrome: Furosemide‐Bicarbonate Therapy

Polycystic Disease and Hepatic Fibrosis in Children

Urologic Aspects of Renal Hypertension

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