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A Haris

Publications and source records attributed to A Haris.

16 recordsLinked to original sources
PubMed2000

[Transtubular potassium gradient in the diagnosis of potassium metabolism disorders].

The transtubular potassium gradient (TTKG) is a simple physiologically based clinical test to study the renal excretion of potassium. This article reviews the most important physiological changes influencing TTKG, the hypokalaemia and hyperkalaemia, the effect of mineralocorticoids, alkalosis, action of diuretics among other drugs etc. The authors studied the abnormalities of TTKG occurring in clinical conditions (renal patients with nephrotic edema, "dry" patients with renal diseases, liver cirrhosis associated with ascites, and primary hyperaldosteronism) and compare them to the results obtained in healthy people. They consider the test to be useful in the recognition of conditions with hypoaldosteronism (including the various types of pseudohypoaldosteronisms and aldosterone resistance) and hyperaldosteronism as well as renal diseases, in accordance with the data published in the literature. On the basis of their own results, they found the method of determination of TTKG informative and helpful also when investigating the site of actions and the effect mechanisms of the diuretics.

Diagnosis, Differential↗
PubMed1999

[Hyperkalemias].

Hyperkalaemia is a frequent electrolyte disturbance connected with new knowledge and practical routine. It is developed by the disorders of the "external balance" (potassium [K] intake and output) as well as the "internal balance" (distribution of K in the extracellular and intracellular fluid compartments). Factors playing a role in it are: the upright posture, physical activity and hyperosmolality. In the hormonal regulation of K metabolism first of all beta adrenergic agents, insulin and aldosterone have significance; the first two mainly in the internal balance. Hyperkalaemia is occurring especially frequently in renal patients (in acute and chronic renal insufficiency, in dialyzed persons) in patients with diabetes, in adrenal insufficiency (Addison's disease, in selective hypoaldosteronisms and in pseudohypoaldosteronisms) in renal tubular acidosis as well as in response to various drugs (ACE inhibitors, angiotensin receptor antagonists, beta blocking agents, potassium sparing diuretics, NSAID's, anticoagulants etc.). Interactions between illness and drugs as well as between drugs and hormones may have outstanding importance in the development of hyperkalaemia. Physical activity carried out in the upright posture in the presence of hyperosmolality (water restriction together with salt or/and glucose loading) developing in pharmacological hypoaldosteronism accompanied with insulin deficiency, may be especially dangerous with respect to hyperkalaemia. To avoid life-threatening hyperkalaemia it is necessary 1. to stop cardiotoxicity with calcium; 2. to enhance K uptake by the cells by bicarbonate, insulin and beta adrenergic agents; and 3. to remove abnormal quantities of K from the body by enemas and/or ion exchange resins. The quickest and best way of treatment of hyperkalaemia is haemodialysis.

Acidosis, Renal Tubular↗
PubMed1999

Patterns of potassium wasting in response to stepwise combinations of diuretics in nephrotic syndrome.

OBJECTIVE: To study the urinary potassium wasting patterns when the decreasing effectiveness of diuretics during repeated administrations are counterbalanced by stepwise increases of doses and combinations of them. PATIENTS: Eleven patients with renal edema. Seven patients suffered from advanced nephrotic syndrome and 4 patients were "forme fruste". METHODS: Urinary excretions and serum levels of potassium, sodium, creatinine, osmoles were determined; specific renal functions, glomerular filtration rate (GFR) fractional excretion of potassium (FE(K)), transtubular potassium gradient (TTKG) and free water reabsorption (TcH2O) were calculated. Nine different intervention-induced changes were followed daily: furosemide (FSD) alone, FSD with chlorthalidone (CTN), "low dose" and "high dose" potassium sparing drugs (PSD), FSD with CTN and "low dose" or "high dose" PSD, and "no drug" as well as "postdiuretic" periods with or without PSD. RESULTS: TTKG significantly decreased in response to FSD. It elevated during FSD with CTN, but remained lower than the baseline. The normal correlation between urinary potassium excretion (UKV) and TTKG became distorted under FSD. UKV and FE(K) were slightly increased by FSD and more markedly when given FSD together with CTN, probably because "distal volume flow" was elevated. In the "postdiuretic" periods TTKG increased, but this was reversed by PSD. In response to PSD, TTKG and UKV decreased, but both were elevated when combining with FSD + CTN. CONCLUSIONS: FSD caused relatively small potassium loss, because the enhanced "distal volume flow" was counterbalanced by a decrease of TTKG. FSD may have had a potassium secretion inhibitory influence as well. Potassium loss and TTKG were enhanced during coadministration of CTN, and decreased by PSD. "Postdiuretic rebound" increase of TTKG was reversed by PSD.

Aged↗
PubMed1998

High-dose phosphate treatment leads to hypokalemia in hypophosphatemic osteomalacia.

The mechanism of the decrease in plasma potassium induced by phosphate treatment was investigated in a 24-year-old hypertensive patient with hypophosphatemic osteomalacia, who was the youngest of four patients, belonging to a 23 number kindred of five generations. Parameters of potassium, sodium, calcium, and phosphate metabolism as well as specific renal functions have been studied in the basal state and during administration of graded doses of phosphate (500-6000 mg). Progressive hypokalemia developed during phosphate treatment. An inverse correlation was found between plasma potassium and doses of phosphate (plasma potassium = -0.2 g phosphate + 3.9 r = -0.49; p < 0.05; N = 21). A renal route of potassium loss was suspected, but could not be confirmed as potassium excretion did not increase although sodium excretion was augmented [basal sodium output: 56.7 mmol/24 h; phosphate treatment: 153 mmol/24 h (p < 0.05)]. Transtubular potassium gradient (TTKG) also decreased and an inverse correlation was found between TTKG and doses of phosphate (r = -0.37; p < 0.02; N = 38). Decrease of TTKG was possibly the result of suppressed K+ secretion. It was concluded that potassium loss occurred by a non-renal (intestinal) route in phosphate-induced hypokalemia. Although major hazards of treatment of hypophosphatemic osteomalacia with phosphate and calcitriol are secondary hyperparathyroidism and vitamin D intoxication, potassium loss also should be kept in mind.

Adult↗
PubMed1997

[Hyponatremia].

Hyponatremia is the most frequent electrolyte disorder. Two forms of it, the "true"--and "pseudo"--hyponatremia are known. The normal osmoregulation is an accurate operation which ensures the steadiness of serum sodium level by regulating vasopressin (ADH) release and water intake. Hyponatremia usually indicates water excess in the body, however, it may be complicated by sodium loss as well. It has hypovolemic, hypervolemic and normovolemic forms; the syndrome of inappropriate antidiuretic hormone (SIADH) is associated mostly with the normovolemic states. Nowadays the pathomechanism, criteria, diagnosis and etiologic factors of SIADH (water intoxication) are fairly well known, but the number of drugs capable of inducing this syndrome is increasing day by day. According to the newest knowledge, SIADH may exist not only in the acute but chronic form as well, which should be born in mind when treating water intoxicated patients. The basic principle is that in cases with mild clinical disturbances aggressive treatment should be avoided. For mild hyponatremia water restriction is usually sufficient, but in serious cases hypertonic saline infusion should be administered. Its speed has to be determined and adjusted carefully according to the needs of the patient, and it can be combined with the administration of furosemide, when necessary. Vasopressin antagonists are under clinical investigation, their therapeutic value has not yet been determined. Water intoxication is not rare-if one keeps it in mind. The syndrome's simple treatment can be life saving for the patient and provides an easy problem solution for the physician.

Acute Disease↗
PubMed1997

[Role of aldosterone in potassium secretion in chronic renal failure associated with hypertension (transtubular potassium gradient)].

Aldosterone protects against hyperkalemia in disorders with reduced number of over-working nephrons. It is not clear however, whether diminished aldosterone production or aldosterone resistance is responsible for the hyperkalemia in chronic renal failure. The importance of this question is underlined by the fact that antihypertensive drugs often reduce aldosterone level. Therefore we investigated the distal tubular potassium "driving force" (transtubular potassium gradient) in 9 patients with chronic renal failure accompanied by hypertension and compared it to the results obtained in 10 healthy persons. Glomerular filtration rate was 15.77 +/- 4.88 ml/min in the chronic renal patients. Serum potassium was normal in 3 of 9 patients, the average 4.88 +/- 0.16 mmol/l, higher than in healthy persons 4.27 +/- 0.09 mmol/l (p < 0.001). Nevertheless the transtubular potassium gradient was lower in patients (3.52 +/- 0.32) comparing to healthy persons (7.25 +/- 0.57, p < 0.001). The patients' plasma aldosterone was much higher than normal. The reduced tubular potassium secretion-decreased "driving force" --suggested to aldosterone resistance. We conclude that the renal tubules' aldosterone resistance is not an exceptional but rather frequent feature in chronic renal failure which should be considered when administering antihypertensive drugs.

Aldosterone↗
PubMed1997

[Adult-onset sex-linked familial hypophosphatemic osteomalacia].

Three patients (a grandmother, her daughter and her grandson) belonging to a 23-number-kindred of five generations suffered from adult-onset, X-linked, familiar hypophosphataemic osteomalacia. According to the familiar anecdotes the great-grandmother also had the same disease. The clinical diagnosis was documented by X-ray pictures, scintigraphic and bone histological results, the laboratory diagnosis was proven by blood and urine analyses examined after phosphate loading. The youngest, 24-year-old patient was treated with daily 3 g phosphate and high doses of calcitriol for 2 years. As a new feature of our therapy, per os treatment with 1.25 micrograms calcitriol was supplemented by daily 2-4 micrograms iv. bolus calcitriol for one week every month. The osteomalacia, causing serious symptoms and complaints, healed. Our treatment seemed to be safe, as renal functions, serum total and ionized calcium and PTH levels (including midnight values) remained in normal range. On the basis of our results this disease can be treated by administration of high doses of phosphate, provided that development of hyperparathyroidism is prevented by the coadministration of high doses of calcitriol.

Adolescent↗
PubMed1996

[Potassium-sparing diuretics (spironolactone, triamterene, amylorid)].

The group of drugs, so-called "potassium sparing diuretics" represent an important part of our modern therapeutic arsenal. Their "weak diuretic" properties are especially beneficial in cirrhotic patients with ascites, when highly effective loop diuretics may be hazardous. Potassium sparing diuretics have not only the advantage of avoiding potassium loss, but can potentiate the effects of diuretics acting in distal tubules and Henle's loop also. They may be combined by each other or ACE inhibitors too, taking the necessary precautions and laboratory monitoring. Their indications include the hypertension and special diseases as Conn's, Bartter's, Liddle syndromes and hirsutism. The broad clinical usefulness justifies the drug inventory ambition to develop new, more effective potassium sparing compounds without side effects. Authors overview their main clinicofarmacological properties, therapeutical indications alone or in combinations and their potential side effects.

Amiloride↗
PubMed1994

[Effect of calcitriol, a vitamin D compound, in bone disease associated with distal renal tubular acidosis].

In a 47-year-old female patient distal renal tubular acidosis (dRTA) led to the development of osteomalacia following 13 years of the first episode of hypokalemic respiratory paralysis and 7 years of KHCO3 treatment. In spite of the musculoskeletal disability, intense bone pain and myopathy, the values of serum calcium (Ca++) and phosphorous (P) showed minimal deviation from the normal levels. The bone scintigraphy was the first indicator of the bone disease. As the disease progressed the serum level of alkaline phosphatase increased gradually and 25-hydroxyvitamin-D level decreased and bone scintigraphy showed multiple areas of increased radioisotope uptake. By that time the patient's condition deteriorated severely, she became almost unable to walk. Rocaltrol (calcitriol) therapy led to dramatic clinical improvement and the complete resolution of the laboratory values. When the alkaline therapy of dRTA does not prevent the development of osteomalacia, administration of a modern vitamin-D preparation can result complete healing of the bone disease.

Acidosis, Renal Tubular↗
PubMed1994

[Atrial natriuretic factor: a "physiological diuretic"].

Investigators are studying for hardly more than 10 years the special role of the atrial natriuretic peptide, "the physiological diuretic", in maintaining of the volume homeostasis. The ANF is synthesized in the atrial granules and also in extra-atrial organs; there are more members of this peptide family: the brain natriuretic peptide, the C-type natriuretic peptide and the urodilatin. The release of ANF is stimulated mainly by atrial wall distension, but some other mechanism may regulate its secretion too. It has regulatory properties on the cardiovascular, renal and endocrine systems. The most important vascular and renal effects of the hormone are as follows: vasodilatation, decrease in blood pressure, increase in glomerular filtration rate, renal blood flow, and filtration fraction, inhibition of sodium and water reabsorption in the proximal and distal renal tubules (natriuresis and diuresis), and decrease in concentrating ability. ANF is the counterregulatory hormone of the renin-angiotensin-aldosterone system. Its other endocrine interactions are complex, mutual stimulation and inhibition between ANF and vasopressin takes place either. The serum level is often elevated in edematous disorders, but there may be tubular resistance to the hormone's action. The therapeutical importance of this "physiologic diuretic" in volume retaining disorders has been proposed, but it needs further studies to establish the clinical therapeutical value of the hormone.

Atrial Natriuretic Factor↗
PubMed1993

Metabolic bone disease (anticonvulsant osteomalacia) and renal tubular acidosis in tuberous sclerosis.

The characteristics triad of tuberous sclerosis-adenoma sebaceum, mental deficiency and epilepsy-associated with distal-type renal tubular acidosis was combined with anticonvulsant osteomalacia in a 41-year-old woman. In addition to the specific bone lesions of tuberous sclerosis, the bone disease was caused by an adverse effect of a drug and possibly also by the renal disorder leading to significant musculoskeletal disability. In response to calcium carbonicum and 1-25-dihydroxyvitamin D therapy the musculoskeletal disability healed and the abnormal biochemical markers of anticonvulsant osteomalacia disappeared. The present observation draws attention to the increased hazard threatening patients on chronic anticonvulsant therapy simultaneously suffering from renal diseases.

Acidosis, Renal Tubular↗
PubMed1992

HTR polymer and sinus elevation: a human histologic evaluation.

HTR (hard tissue replacement) polymer was used in a second session to perform 26 sinus floor elevations in 16 patients with dental implantation (Flexiroot, U.S.A.). A period of 6, 8, 10, or 12 months elapsed between the two operations, making it impossible to examine the tissular integration of HTR from both clinical and human histologic aspects. Following the sinus elevation, neither prolonged wound healing nor a rejection reaction was observed in any of the cases. During an 8 to 10 month period, sufficient new bone and fibrous connective tissue had grown between the HTR granules to ensure appropriate supporting tissue for the implantation. Subsequently (12 months), the HTR and the new bone became clinically increasingly harder, forming a union that was difficult to shape. HTR may be stated to be a material suitable for purposes of sinus elevation. In three cases in which the alveolar bone was originally very thin (2 to 3 mm), the resorption of this bone was observed, as a consequence of this the implantation was not performed. The resorption is explained by the inadequate blood supply that developed for surgical-technical reasons, and is not connected with the nature of the material used for the sinus elevation.

Alveolar Bone Loss↗
PubMed1991

[Experience with the clinical use of HTR (hard tissue replacement) polymer. Sinus elevation, human histological studies].

The HTR polymer was employed under clinical circumstances. Results supported that the HTR polymer may well be employed for bone replacement. The forming of the support tissue between the plastic granulums has been accompanied with biopsies. Though in some cases giant cell reaction of alien body type have been observed, yet this has never been of such degree that it would have impeded the reception of the stuff. According to the authors opinion after reinforcement of the lower wall of the facial cavity with HTR polymert in 8 to 10 months an enduring suitable support tissue is formed.

Adult↗
PubMedDate not supplied

Familial adult onset X-linked hypophosphataemic osteomalacia (report of a family; clinical and experimental studies).

From four patients (a great-grandmother, grandmother, her daughter and her grandson) suffering from a very severe form of familial X-linked hypophosphataemic osteomalacia (XLH), belonging to a 23-number-kindred of five generations, the youngest patient a 24-year-old man with an adult onset XLH was treated with phosphate and calcitriol for two years. Phosphate was given in increasing doses (500-6000 mg elemental phosphate) by mouth for a relatively short-term period and calcitriol in high doses per os combined with intermittent intravenous administration. Long-term treatment consisted of daily three grams of phosphate and 1.25 micrograms calcitriol by mouth combined with daily 2 micrograms calcitriol intravenously for one week every month. Dramatic clinical improvement occurred accompanied with definite radiological and scintigraphical changes. Serum phosphate increased from 0.525 +/- 0.478 mmol/l to 1.054 +/- 0.041 mmol/l (p < 0.001) in response to 3000 mg phosphate. A close correlation (r = 0.69) was found between serum phosphate and urinary phosphate excretions (p < 0.001) and an inverse correlation (r = -0.31) was found between serum phosphate and tubular reabsorption of phosphate (p < 0.01). Serum and urinary calcium values, parathormone as well as renal functions did not change. Administration of high doses of phosphate seemed to be an effective and probably safe form of treatment in XLH provided that development of hyperparathyroidism is prevented by the coadministration of high doses of calcitriol.

Adult↗