text: Nephrolithiasis  is a common condition encountered in emergency rooms and also as an outpatient in the primary care setting. Its incidence and prevalence is increasing both in women and men, with women slightly incraing recently due to obesity and lifestyle changes. Nephrolithiasis may be classified into 4 subtypes/groups: calcium stones, struvite stones, uric acid stones and cystine stones. The common causes of nephrolithiasis include hypercalcemia, hyperparathyroidism, hypercalciuria, infection with urea splitting microorganisms like Proteus and Pseudomonas, gout, dehydration, inflammatory bowel disease. Less common causes of nephrolithiasis include drugs such as loop diuretics, Acetazolamide, ciprofloxacin, indinavir, guaifenesin triamterene and magnesium trisilicate. It is understood that nephrolithiasis is the result of combination of different mechanism responsible for different types of stones. Calcium stones are the most common type of<unk> s. Approximately 80% of all calcium stones are calcium oxalate stones. The pathophysiology of calcium stones is complex and involves dietary concerns, hypercalciuria, hypocitaturia, hyperoxaluria, hyperuricosuria and biomineralization. The underlying pathophysiological mechanisms responsible for uric acid stones are low urine volume, hyperuricosuria and high acidic urine. Cystinuria is a rare hereditary gene disorder which causes impaired renal reabsorption of cationic amino acids and cystine. It is caused by mutations in either of the two subunits (rBAT(SLC3A2) and b0,+AT(SLC7A9)) forming cystine stones. Struvite stones are usually seen in patients which have infection with urease +ve organisms. Urine pH is usually alkaline (>7.2). Nephrolithiasis can be passed on to following generations due to rare causes of hypercalciuria such as hereditary distal renal tubular acidosis, dent disease, Bartter syndrome types III and IV, autosomal dominant hypocalcemic hypercalciuria and familial hypomagnesemia. Nephrolithiasis associated with Hyperparathyroidism, Gout, Hypocitaturia, Sarcoidosis, chronic urinary tract infections and Obesity.On gross pathology, the characteristic findings of nephrolithiasis include location = 80% unilateral, usually in calyces, pelvis or bladder. The size=variable, 2-3 mm usually. All stones contain an organic matrix of mucoprotein. The shape of struvite stone is staghorn shaped. On microscopic histopathological analysis, the characteristic findings of nephrolithiasis include different shapes of stones/crystals are such as cystine= hexagonal, struvite= coffin lid shape, calcium oxalate= pyramid shape to dumbbell shape and uric acid= rectangular/rhomboidal. Oxalate crystals are highlighted by polarized light. Also, foreign body giant cells and macrophages are seen with the stones.It has increased from every 1 in 20 to 1 in 11 person in United States has<unk> s. If left untreated, <30% of patients with nephrolithiasis may progress to develop renal colicky pain due to increase in rate of growth.Most of the stones pass spontaneously. about 10-20% of symptom-causing stones fail to pass. Lower poles stones were significantly less likely to cause symptoms or pass spontaneously. They can progress to hydronephrosis especially when combined or superimposed by urinary tract infection. Common complications of nephrolithiasis include hydronephrosis, chronic renal failure, hypertension, cardiovascular disease, and increased risk of fracture. Prognosis is generally excellent. Approximately 80-85% resolve spontaneously. Recurrence rates for calcium stones after the initial event is 40–50% at the end of 5 years and 50–60% at the end of 10 years.The patients with nephrolithiasis may have a positive history of flank pain. Common symptoms of nephrolithiasis include flank pain progressing downward and anteriorly into the groin as the stone moves, hematuria, nausea and vomiting urinary frequency and urgency. Less common symptoms include burning micturition. Patients with nephrolithiasis usually appear in pain and trying to achieve a comfortable position. Common physical examination findings of nephrolithiasis include costovertebral angle tenderness, may accompany fever with increased heart rate and respiratory rate. They can have hypoactive bowel sounds due to ileus caused by severe pain. They can have hematuria in microscopic exmaination. Laboratory findings consistent with the diagnosis of nephrolithiasis include hypercalcemia, hypercalciuria, hyperoxaluria, hypocitraturia, hyperuricemia and hyperuricosuria. Abdominal ultrasound may be helpful in the diagnosis of nephrolithiasis Findings on an ultrasound suggestive of/diagnostic of nephrolithiasis include: echogenic or hyperechogenic foci, acoustic shadowing, twinkle artefact on colour Doppler, colour comet-tail artefact , and increased resistive index which signifies acute obstruction. CT scan is the gold standard test for the diagnosis of nephrolithiasis. Abdominal and pelvic CT scan is helpful in the diagnosis of nephrolithiasis. Findings on CT scan diagnostic of nephrolithiasis include radiopacity showing the location, density and composition of stones calcium oxalate +/- calcium phosphate: 400-600 HU, struvite (triple phosphate): usually opaque but variable, pure calcium phosphate 400-600 HU, uric acid: 100-200 HU and cystine: opaque. The treatment of nephrolithiasis involves different measures e.g non pharmacological measures consisting of increased fluid intake, straining an dietary restrictions. Pharmacological measures include pain relief using NSAIDs and opioids., helping passage of stone spontaneously with drugs like tamsulosin and nifedipine. The treatment of underlying cause and being specific to type of stones is very important.It involves treating primary hyperparathyroidism and Renal tubular acidosis. For those having high urinary calcium, Hydrochlorothiazide or Chlorthalidone are used. For recurrent stones and high urine uric acid, Allopurinol is used. For recurrent stones and hypocitraturia, Potassium citrate is sued to alkalinize the urine. For uric acid stones, alkalinizing urine with potassium citrate/potassium bicarbonate is done and if needed Allopurinol is also used. For struvite stones, medical therapy is not of much help, although urease inhibitors such as acetohydroxamic acid can be given in urease +ve etiology. For cysteine stones, again alkalinizing urine helps along with Tiopronin. The Urological consult is needed when stone >10 mm in diameter, uncontrolled pain, Anuria, or there is Acute<unk>  injury. The mainstay of treatment for nephrolithiasis is medical therapy. Surgery is usually reserved for patients with either persistent and severe pain, renal failure,<unk>  infection and when stone fails to pass or move after 30 days. The surgeries which are being used currently include extracorporeal shockwave lithotripsy, ureteroscopy and percutaneous nephrolithotomy. Effective measures for the primary prevention of nephrolithiais include diet control and high fluid intake. Effective measures for the secondary prevention of nephrolithiasis include measures to prevent recurrence of the stones and prevent complications. It includes measures like correcting hydration and dietary habits. Drugs like allopurinol to prevent hyperuricemia, potassium citrate to alkalinize the urine and avoidance or judicious use of diuretics.
option_0: Kidney stone
option_1: Nephrolithiasis
option_2: Bladder stone
option_3: Kidney abscess
option_4: Renal colic
option_5: Pyonephrosis
option_6: Pyelonephritis
option_7: Renal cyst