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Query: UMLS:C0152169 (renal colic)
 811 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty male patients with urolithiasis (UL), associated with idiopathic hypercalciuria (IH), were studied in comparison to a group of 18 male normocalcemic patients with inactive calcium stone disease of unknown etiology. In the group of IH-UL, in addition to hypercaliuria, statistically significant hyperphosphaturia with decreased tubular reabsorption of phosphate and hyperuricemia were observed; there was a tendency to hypophosphatemia although non-significant. In 36% of the IH-UL patients the first episode of renal colic appeared at age 40 to 50. Thirty-eight per cent of the IH-UL patients had recurrent stone formation. Twenty per cent of the IH-UL patients had a family history of urolithiasis. Forty-six per cent of all stones contained oxalate in addition to calcium, and 25% of the stones contained oxalate and phosphate.
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PMID:Urolithiasis associated with hypercalciuria. 60 17

On about one fourth of the patients ureteral colics caused by oxalate and phosphate calculi lead to a reversible hyperuricemia. This result seems to be important, because we might wrongly diagnose a uric acid calculus. The reason for hyperuricemia is a temporary diuretic disturbance of the uric acid. It cannot be explained by the functional loss of the obstructed kidney, because a nephrectomy does not change the uric acid level. As a possible reason we suppose a ketose by food deficiency and vomiting caused by renal colic.
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PMID:[Reversible hyperuricemia in case of ureteral colics (author's transl)]. 115 68

A prospective multicenter study was designed to determine the frequency and prognostic importance of hypercalciuria in children with hematuria. Urinary calcium excretion was examined in 215 patients with unexplained isolated hematuria (no proteinuria, urolithiasis, infection or systemic disorder). Hypercalciuria (urinary calcium excretion greater than 4 mg/kg/day) was identified in 76 patients (35%). Compared to patients with normal urinary calcium excretion, children with hematuria and hypercalciuria were characterized by male preponderance, white race, family history of urolithiasis, gross hematuria and calcium oxalate crystals. Renal biopsies were performed in 10 patients with urinary calcium excretion 0.4 to 2.5 mg/kg/day; three had IgA glomerulonephritis, three had glomerular basement membrane thinning, one had proliferative glomerulonephritis and three were normal. Renal biopsies in three patients with hypercalciuria showed focal segmental glomerulosclerosis, hereditary nephritis or no abnormalities. Oral calcium loading tests showed renal hypercalciuria in 26 patients, absorptive hypercalciuria in 15 patients and were not diagnostic in 35 patients. Serum parathyroid hormone, bicarbonate and phosphorus and urinary cyclic adenosine monophosphate concentrations were similar in the three groups of hypercalciuric patients. Urinary calcium excretion after one week of dietary calcium restriction was higher (5.8 mg/kg/day) in renal hypercalciuria than in other hypercalciuric patients (3.4 mg/kg/day), P less than 0.01. One to four years follow-up was available for 184 patients. Eight of 60 hypercalciuric patients developed urolithiasis or renal colic compared to 2 of 124 patients with normal urinary calcium excretion (P less than 0.001). Hypercalciuria is commonly associated with isolated hematuria and represents a risk factor for future urolithiasis in children with hematuria.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Idiopathic hypercalciuria: association with isolated hematuria and risk for urolithiasis in children. The Southwest Pediatric Nephrology Study Group. 240 91

A group of 28 Syrian children (19 males and 9 females; age ranging from 2.5 to 12 years) were diagnosed clinically and radiologically to have upper urinary tract stones. The commonest presentations were renal colic, vomiting, haematuria, pyrexia and vague abdominal pain. Family history of renal stones was present in 21% of cases. Haematological picture and chemical analysis of blood were within the normal limits for their age and sex. Urine analysis, however, showed significantly marked increase in the 24-hour excretions of calcium and uric acid. Microscopic examination showed haematuria and pyuria in 72% of the children with urolithiasis. Chemical analysis of removed stones revealed that most of them were mixed stones of calcium oxalate and urate or/and phosphate. Pure stones of calcium oxalate or calcium phosphate were less common. Radiologically, about 95% of all stones were demonstrated by plain X-ray, while 5% only after IVP.
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PMID:Some features of paediatric urolithiasis in a group of Syrian children. 358 9

To determine the optimal time at which to assess the urinary risk factors for calcium stone formation, we followed 11 patients after an episode of acute renal colic with sequential 24-hour urine collections, first in the hospital and then at regular intervals after they were discharged from the hospital. The changes that occurred in the urinary risk factors were compared to those of a control group in which samples were collected during the same interval. The in-hospital 24-hour urine volumes were high but decreased gradually to approach the relatively constant volume of the control group by 3 months. The opposite trend occurred with respect to the 24-hour urinary excretion of calcium. There were no significant changes in the 24-hour urinary pH or excretions of oxalate, uric acid and alcian blue precipitable polyanions. The over-all effect was to cause a progressive increase in the probability of stones forming in the patients. The accurate assessment of the urinary risk factors of calcium stone disease requires at least a 3-month delay following acute renal colic. This delay usually will provide sufficient time for the stone to pass and for the patient to return to the normal dietary and fluid intake.
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PMID:When should patients with symptomatic urinary stone disease be evaluated metabolically? 650 4

Acute episodes of renal colic are associated with severe pain and often necessitate invasive procedures and costly absences from work. A medical approach to evaluate all patients with kidney stones is generally recommended to detect underlying systemic disorders associated with nephrolithiasis and prevent further stone formation. patients with a single stone require a limited evaluation, whereas those with metabolically active stones, stones not composed of calcium oxalate, all children, and patients in demographic groups not commonly associated with nephrolithiasis should undergo a more extensive workup. The major classes of stones formed are calcium oxalate, calcium phosphate, uric acid, struvite, and cystine. This article focuses on etiologic factors that predispose to nephrolithiasis in general, as well as to specific stone types. A thorough review of the evaluation and therapy required for all stones is presented.
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PMID:Clinical approach to adults. 889 Mar 94

The primary care physician has a responsibility not only to recognize and treat acute stone passage but to ensure that the patient with recurrent stones has metabolic evaluation and appropriate preventive care. Renal colic is typically severe, radiates to the groin, is associated with hematuria, and may cause ileus. About 90% of stones that cause renal colic pass spontaneously. The patient with acute renal colic should be treated with fluids and analgesics and should strain the urine to recover stone for analysis. Highgrade obstruction or failure of oral analgesics to relieve pain may require hospitalization; a urinary tract infection in the setting of an obstruction is a urologic emergency requiring immediate drainage, usually with a ureteral stent. Several approaches are available when stones do not pass spontaneously, including extracorporeal shock wave lithotripsy, percutaneous lithotripsy, and ureteroscopic laser lithotripsy. Calcium stone disease has a lifetime prevalence of 10% in men and causes significant morbidity. Renal failure is unusual. Stone types include calcium oxalate, uric acid, struvite, and cystine. Stone analysis is particularly important when a noncalcareous constituent is identified. The majority of patients with nephrolithiasis will have recurrence, so prevention is a high priority. High fluid intake is a mainstay of prevention. Metabolic evaluation will indicate other appropriate preventive measures, which may include dietary salt and protein restriction, and use of thiazide diuretics, neutral phosphate, potassium citrate, allopurinol, and magnesium salts. Dietary calcium restriction may worsen oxaluria and negative calcium balance (osteoporosis).
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PMID:Nephrolithiasis: acute management and prevention. 965 69

Annual incidences of kidney stones are about 0.1-0.4% of the population, and lifetime prevalences in the USA and Europe range between 8 and 15%. Kidney stones occur more frequently with increasing age and among men. Within ten years, the disease usually recurs in more than 50% of patients. Nowadays, about 85% of all kidney stones contain calcium salts (calcium oxalate and/or calcium phosphate) as their main crystalline components. Because human urine is commonly supersaturated with respect to calcium salts as well as to uric acid, crystalluria is very common, i.e. healthy people excrete up to ten millions of microcrystals every day. Recurrent stone formers appear to excrete lower amounts or structurally defective forms of crystallization inhibitors which allows for the formation of large crystal aggregates as precursors of stones. Alternatively, crystal adhesion to urothelial surfaces may be enhanced in stone formers. Medical treatment of renal colic is based on nonsteroidal antiinflammatory drugs, because prostaglandins appear to play a crucial role in the pathophysiology of pain during ureteral obstruction. In addition, centrally acting analgesics such as pethidine-HCl may be required in many cases. The administration of high amounts (3-4 liters/day) of intravenous fluids should be abandoned, since it may raise intraureteral pressure whereby pain increases and kidney pelvis or fornices may rupture. All first-stone formers should undergo a simple basic evaluation, including stone analysis (x-ray diffraction or infrared spectrometry), serum values of ionized calcium (alternatively: total calcium and albumin) and creatinine, urinalysis and repeated measurements of fasting urine pH in order to detect urinary acidification disorders or low urine pH. In high-risk patients with as first stone episode (i.e. strongly positive family history, inflammatory bowel disease, short-bowel syndrome, nephrocalcinosis, bilateral stones, hypercalcemia, renal tubular acidosis, airline pilots) as well as in all recurrent stone formers, an extended metabolic evaluation should be performed. Two 24-hurines should be collected on free-choice diet not prior to three months after stone passage or urological intervention. Analysis includes measurements of volume, creatinine, calcium, oxalate, uric acid and citrate; sodium and urea as markers of salt and protein consumption are optional but clinically very helpful. Since hypercalciuria is of much less importance than increases in urinary oxalate, therapeutic efforts should primarily focus on lowering urinary oxalate excretion. Sufficient calcium intake, i.e. 1200 mg per day, is crucial, because it allows for binding of oxalate at the intestinal level whereby increases of urinary oxalate (reciprocal hyperoxaluria) can be avoided. Excess intake of flesh protein (meat, fish, poultry) is lithogenic since it increases urinary calcium, oxalate and uric acid, and lower citrate. On the other hand, a diet rich in alkali (vegetables, fruit) is associated with a lower risk of stone formation. A "common sense diet" containing sufficient amounts of fluids, 1200 mg of calcium per day and reduced amounts of flesh protein as well as salt is able to reduce the 5-year stone recurrence rate in calcium stone formers by 50%. The scientific evidence for drug treatment (thiazides, alkali citrate) is rather poor: the most widely quoted randomized thiazide trial included only 42 patients of whom 36% left the protocol prematurely, whereas 36-48% of patients included in three randomized studies with alkali citrate suffered from undesirable side-effects; nevertheless, citrate therapy reduced the stone recurrence rate by 38%, compared with 22% in patients on placebo treatment (p < 0.0005).
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PMID:[Pathophysiology, diagnosis and conservative therapy in calcium kidney calculi]. 1264 86

A 70-year-old woman was admitted in the Department of Nephrology because of renal insufficiency. Six years previously, as consequence of a venous mesenteric thrombosis, she underwent an extense intestinal resection with subsequent short intestine syndrome. Five years after the surgery an increase in the creatinine concentration was observed (1.4 mg/dl). One year later, it increased up to 3.1 mg/dl and the patient was remitted to our Department. The radiological study revealed calcifications on both kidney silhouettes. In the next year, renal function worsened and the calcifications increased. Coinciding with the beginning of the chronic hemodialysis treatment she suffered a renal colic with passage of a calcium oxalate stone.
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PMID:[Chronic renal failure secondary to hyperoxaluria following small bowel syndrome]. 1705 63

Nephrolithiasis treatment has become easier and less invasive with the development of extracorporeal shockwave lithotripsy (SWL) and endourologic techniques. However, medical therapy represents a well-established and complementary approach that can improve the efficacy of SWL and endourology. During recent decades, pharmacologic intervention has become more effective in stone disease: drugs can control the pain of renal colic, interfere at various levels in lithogenesis, and contribute to the expulsion of stones. It is well known that lithogenesis is a multifactorial process influenced by environmental-nutritional factors (low urinary volume, diet rich in animal protein, etc) and metabolic alterations; i.e., hypercalciuria, hyperuricosuria, and deficiency of stone-inhibiting factors (citrate, magnesium, glycosaminoglycans [GAGs]). Specific drugs such as citrate, allopurinol, and thiazide represent highly effective treatments for the promoting factors. Furthermore, recent findings suggest an interesting role for a phytotherapeutic agent, Phillantus niruri, and its inhibitory action on calcium oxalate crystallization related to the higher incorporation of GAGs into the calculi. Another step forward in medical management of stone disease is expulsive therapy. Many studies have proven the efficacy of medical expulsive therapy with nifedipine and alpha-blockers: their specific action on ureteral smooth muscle in association with anti-edema drugs accounts for their efficacy in expelling ureteral stones. In this paper, we provide an update on the medical treatment of stone disease, focusing our attention on what is known and what is new in renal colic and litholithic and expulsive medical therapy.
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PMID:Medical therapy of urolithiasis. 1714 48


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