Gene/Protein Disease Symptom Drug Enzyme Compound
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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 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

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

We retrospectively reviewed the presentation and management of children with primary hyperparathyroidism (PHPT) from 1973 to 1995 at a paediatric tertiary-care centre. There were 11 patients (6 females), aged 12.3-17.7 years at presentation, with sporadic PHPT confirmed by histopathology (single adenoma). Presentation consisted of renal colic, or non-specific gastrointestinal, musculoskeletal or neurological symptoms. Misdiagnosis was common until hypercalcaemia was identified, 0.5-24 months after onset of symptoms (mean 7.7 months). All patients had hypercalcaemia and low-normal serum phosphate. The parathyroid hormone (PTH) radioimmunoassay used before 1986 was elevated in 1/4 patients; the intact PTH assay used after 1986 was elevated in 7/7 patients. At presentation, six had end-organ damage: band keratopathy, renal lesions, and/or bone disease. Preoperative localization was accurate in 0/4 patients diagnosed before 1986, but 5/7 patients diagnosed after 1986: three by ultrasound or sestamibi scan alone, and two by ultrasound and technetium scan. Surgical outcome was not dependent upon the accuracy of pre-operative localization. PHPT is rare in children but usually associated with end-organ damage, presumably due to delayed diagnosis. It should be considered in the differential diagnosis of unexplained non-specific complaints. The intact PTH assay greatly assists pre-operative diagnosis. The usefulness of pre-operative localization requires further research.
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PMID:Primary hyperparathyroidism in a paediatric hospital. 901 86

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

This report describes the clinical and biologic data and bone density measurements in 19 adults seen in a rheumatology department, with phosphate diabetes defined by low serum phosphate levels and decreased tubular reabsorption of phosphate in the absence of known etiology. There were 14 males and 5 females with a mean age at disease onset of 36.7 years (20-68 years) and at diagnosis of 43.9 years (24-70 years). Axial pain was present in 17 patients (90%), radicular pain in 13 patients (68%), pain at night in 14 patients (74%), fatigue in 7 patients (37%), myalgia in 6 patients (32%), fracture in 6 patients (32%), renal colic in 4 patients (21%) and depression 10 patients (53%). Mean serum phosphorus was 2.25 mg/dL (1.08-2.76); maximum tubular reabsorption of phosphate/glomerular filtration rate was 0.58 (0.4-0.76) (n > 0.77). Calcium/creatinine > 0.48 was seen in 9 patients (47%), indicating an associated hypercalciuria. Serum calcium, sodium, magnesium, creatinine, cortisol, T3, T4, thyroid-stimulating hormone (TSH), 25 and 1,25 OH2 vitamin D3 were normal. Glucose and amino acid were absent from urine. Bone mineral density at L2-L4 level (Z-score) was -2.13 (-0.9 to -4.25), and at the femoral neck was -1.34(-1.5 to -3.2). Bone biopsy in 5 patients showed osteoporosis with minor osteoid deposition.Idiopathic phosphorus diabetes (IPD) is a rheumatic disease with chronic axial pain at night, radiculitis-like symptoms, fatigue and depression. In half of the patients, IPD is associated with hypercalciuria. Bone mineral density at L2-L4 and femoral neck level is low. Bone biopsies show osteoporosis. Chronic pain, fatigue and depression resulting from IPD may be improved by treatment with oral calcitriol and phosphorus. There might be a delay in improvement of a few months, even if the blood phosphate level is normalized. A 3% increase in bone mineral density could be measured at 6-month intervals when blood phosphate was maintained. This disease is often misdiagnosed when the maximal reabsorption rate of phosphorus is not calculated.
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PMID:Adult onset idiopathic phosphate diabetes. 1907 33

Renal stone disease often begins by renal colic. In order to manage this event adequately, several goals should be pursued: first, attenuate pain; second, favour progression and spontaneous expulsion of stones; third, prevent from obstructive and infectious complications. All of the aforementioned points pertain to medical management of this disease. Concerning prevention, it is widely agreed that pathogenesis of kidney stones is a consequence of abnormalities in urine environment, leading to a disequilibrium between promoters and inhibitors of crystallization. Therefore, the rationale for therapy is to make urine less conductive to stone formation, by both decreasing state of saturation and increasing inhibitory potential. In only some types of stone-forming salts it is possible to obtain undersaturation with the solid phase. Indeed, uric acid stones can be chemically dissolved by using alkali and allopurinol. To a lesser extent, this also applies to cystine stones, with the use of thiols and alkali. In these subsets, the aforementioned tools are also effective to prevent new stone formation. Much more challenging appears the treatment of calcium containing stones. About 10% of such stones is caused by systemic disorders and, in these cases, the prevention of new stones is successfully accomplished by curing the underlying disease. For instance, parathyroidectomy cures calcium nephrolithiasis in case of hyperparathyroidism. However, the majority of patients with calcium stones are idiopathic stone-formers, in whom metabolic abnormalities often occur, namely, hypercalciuria, hyperoxaluria, hypocitraturia. The correction of these abnormalities by using thiazide diuretics, alkaline citrates, potassium phosphate and bisphosphonates is based on the prevailing metabolic defect. Among the most recent available tools, Oxalobacter Formigenes and probiotics have been proposed to treat primary or secondary hyperoxalurias. In general, the treatment of stone disease reduces its recurrence rate, but only seldom results in stable remission. Anyway, less stones mean reduction of the need for urological procedures and the associated infective or obstructive complications. Of course, medical prevention implies financial efforts, but a careful cost to benefit analysis demonstrates that these are well justified.
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PMID:Use of drugs for nephrolithiasis. 2246 Sep 95

Renal stone disease is characterized by the differences depending on the age, gender, and the geographic location of the patients. Seventy-five percent of the renal stone components is the calcium (Ca). The most common type of the stones is the Ca oxalate stones, while Ca phosphate, uric acid, struvite, and sistine stones are more rarely reported. Other than these types, triamterene, adenosine, silica, indinavir, and ephedrine stones are also reported in the literature as case reports. However, to the best of our knowledge, aluminum hydroxide stones was not reported reported before. Herein we will report a 38-years-old woman with the history of recurrent renal colic disease whose renal stone was determined as aluminum hydroxide stone in type. Aluminum mineral may be considered in the formation of kidney stones as it is widely used in the field of healthcare and cosmetics.
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PMID:A case of recurrent renal aluminum hydroxide stone. 2501 40


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