pituitrin and Kidney-Calculi

In 85% of patients, renal colic is caused by renal-ureteral stones with extrinsic obstructions such as pelvic, retroperitoneal or intestinal abnormalities, and intrinsic reno-ureteral obstructions, e.g. junction pathologies and malformation, accounting for only 10 and 5%, respectively. The objectives of therapy for renal colic therapy are to eliminate pain, preserve renal function and eliminate the obstruction by the excretory pathway. Many drugs can be used to relieve pain: non-steroid anti-inflammatory agents (NSAIDs), opioid analgesics, antidiuretic hormone (ADH), loco-regional anesthesia and acupuncture. Opiates are the first-choice therapy during pregnancy as no other drug is indicated because of tetragenic potential. Paracetamol (N-acetyl-p-aminophenol) is the only NSAID that is registered for pediatric use because it has none of the adverse side effects that are associated with NSAIDs. Tamsulosin, an alpha-lithic drug, has very recently been included among the drugs that are used for stone expulsion. The rationale underlying its use is that a high concentration of alpha-1D adrenergic receptors has been recently detected in the terminal ureter, especially in the intramural tract. Inhibition of alpha-1D receptor stimulation should relax smooth muscle in the intramural ureteral tract, making stone expulsion easier.

Topics: Acute Disease; Analgesics, Opioid; Anti-Inflammatory Agents, Non-Steroidal; Female; Humans; Kidney Calculi; Male; Pain Measurement; Prognosis; Risk Assessment; Severity of Illness Index; Treatment Outcome; Ureteral Calculi; Vasopressins

The clinical manifestations of drug-induced renal disease may include all the manifestations attributed to natural or spontaneous renal diseases such as acute renal failure, chronic renal failure, acute nephritic syndrome, renal colic, haematuria, selective tubular defects, obstructive nephropathy, etc. It is therefore vital in any patient with renal disease whatever the clinical manifestations might be, to obtain a meticulous drug and toxin inventory. Withdrawal of the offending drug may result in amelioration or cure of the renal disorder although in the case of severe renal failure it may be necessary to utilise haemodialysis or peritoneal dialysis to tide the patient over the period of acute renal failure. Analgesic nephropathy is an important cause of terminal chronic renal failure and it is therefore vital to make the diagnosis as early as possible. The pathogenesis of some drug-induced renal disorders appears to be immunologically mediated. There are many other pathogenetic mechanisms involved in drug-induced renal disorders and some drugs may under appropriate circumstances be responsible for a variety of different nephrotoxic effects. For example, the sulphonamides have been incriminated in examples of crystalluria, acute interstitial nephritis, acute tubular necrosis, generalised hypersensitivity reactions, polyarteritis nodosa and drug-induced lupus erythematosus.

Topics: Acute Disease; Analgesics; Humans; Hypercalcemia; Immune System Diseases; Kidney Calculi; Kidney Concentrating Ability; Kidney Diseases; Kidney Tubular Necrosis, Acute; Necrosis; Nephrosis; Nephrotic Syndrome; Potassium Deficiency; Proteins; Tetracyclines; Ureteral Diseases; Ureteral Obstruction; Urologic Neoplasms; Vascular Diseases; Vasopressins

Topics: Angiography; Biological Transport, Active; Contrast Media; Dehydration; Diuresis; Furosemide; Glomerular Filtration Rate; Humans; Hypertension; Kidney; Kidney Calculi; Kidney Concentrating Ability; Kidney Failure, Chronic; Kidney Tubules; Male; Metaraminol; Prostatic Diseases; Renal Artery Obstruction; Sodium; Urinary Calculi; Urography; Vasopressins

Topics: Adult; Benzazepines; Cystinuria; Female; Humans; Kidney Calculi; Male; Middle Aged; Secondary Prevention; Tolvaptan; Vasopressins

Topics: Adrenal Insufficiency; Adult; Amputation, Surgical; Anti-Bacterial Agents; Disseminated Intravascular Coagulation; Epoprostenol; Escherichia coli; Escherichia coli Infections; Female; Gangrene; Humans; Hydrocortisone; Hypotension; Kidney Calculi; Leg; Metatarsus; Pain; Platelet Aggregation Inhibitors; Purpura Fulminans; Shock, Septic; Vasopressins

A 60-year-old woman who had been instructed to increase her water intake because of nephrolithiasis developed the syndrome of inappropriate secretion of antidiuretic hormone when treated with chlorthalidone for mild hypertension. Serum osmolality was 235 mOsm/kg with concomitant urine osmolality of 490 mOsm/kg. When serum sodium decreased to 110 mEq/liter, plasma antidiuretic hormone (ADH) was elevated at 30 pg/ml. The syndrome resolved when chlorthalidone was discontinued together with fluid intake restriction. Plasma ADH returned to normal (less than 0.5 pg/ml) after three days of treatment. The favorable outcome in this patient is attributed to early recognition of the syndrome, which might occur even with nonthiazide diuretics such as chlorthalidone.

Topics: Chlorthalidone; Female; Humans; Hypertension; Kidney Calculi; Osmolar Concentration; Sodium; Time Factors; Vasopressins

Topics: Acid-Base Equilibrium; Bicarbonates; Blood Glucose; Blood Urea Nitrogen; Chlorides; Creatinine; Diuresis; Fludrocortisone; Humans; Kidney; Kidney Calculi; Kidney Tubules, Proximal; Magnesium; Male; Middle Aged; Natriuresis; Osmolar Concentration; Peritoneal Dialysis; Phosphates; Plasma Substitutes; Potassium; Sodium; Urea; Uric Acid; Vasopressins; Water-Electrolyte Balance