It is understood that nephrolithiasis is the result of combination of different mechanism responsible for different types of<unk> s. Calcium<unk> s are the most common type of<unk><unk> s.  Approximately 80% of all calcium<unk> s are calcium oxalate<unk> s. The pathophysiology of calcium<unk> s is complex and involves dietary concerns, hypercalciuria, hypocitaturia, hyperoxaluria, hyperuricosuria and biomineralization. The underlying pathophysiological mechanisms responsible for uric acid<unk> s 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<unk> s. Struvite<unk> s 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<unk> s contain an organic matrix of mucoprotein. The shape of struvite<unk>  is staghorn shaped. On microscopic histopathological analysis, the characteristic findings of nephrolithiasis include different shapes of<unk> s/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<unk> s.
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