Nephrolithiasis • Calcium oxalate (and to some degree calcium phosphate) stones account for 80% of all kidney stones • Remaining stones are uric acid (10%), struvite (10-15%) and cystine (1%) stones • It is possible for patient to have multiple stones and for them to be more than one type of stone Risk Factors • Crystallization occurs when otherwise soluble solutes precipitate due to supersaturation or changes in urinary pH, protein content, or due to reaction with other solutes • Crystals cause epithelial injury, deposition of stone formation, bleeding, obstruction, and pain • Frequently identified risk factors include hypercalciuria, hyperoxaluria, hypocitraturia, decreased calcium intake, increased oxalate intake, increased animal protein intake, and decreased hydration • There is more than 2-fold increase in risk of kidney stones with positive family hx of kidney stones • Patients with history of kidney stones have a 10-30% 3-5 year recurrence rate • 25% of people with gout will get kidney stones Signs and Symptoms • Classic presentation is severe acute intermittent flank pain lasting 20-30 minutes per episode with radiation to the groin, testicles, or vulva, often with hematuria • CVA tenderness is found in approximately 50% of patients with kidney stones • Rebound tenderness is found in 29% and guarding in 61% • Nausea and vomiting is present in 50% of the patients • Microscopic hematuria is present in 85% of patients; gross hematuria is seen in 30% of cases • Frequency, urgency and dysuria occur in 3-24% of patients • Poor outcomes are associated with diabetes, hypertension, renal insufficiency, history of complicated stone disease, urinary tract instrumentation, urinary tract infection, and single, transplanted or horseshoe kidney Does Stone location affect rates of passage? Stone Location % Spontaneous passage rate proximal ureter 48 mid-ureter 60 distal ureter 75 ureterovesical junction • Most stones that pass spontaneously pass within 1 month of symptom onset. • Who can be discharged home without urology consult? • small stones, symptoms resolved, no evidence of infection • Discharge Instructions o Rx for NSAIDs or opioids or combination therapy +/- MET therapy o Instructions to return for fever, vomiting, worsening pain, decreased urine output, nausea, and/or chills o If stone has not passed, provide patient with strainer to collect stone for outpatient analysis o Urology follow-up Renal Injury in the Setting of Nephrolithiasis Nephrolithiasis is not always a benign process and it’s important for the physician to identify which stones require urgent or emergent attention in order to optimize patient care. A literature review by Tang et al. noted that nephrolithiasis plays a role in causing kidney damage by mechanisms, which include 1. post-obstructive acute kidney injury 2. direct cellular toxicity 3. chronic kidney disease (CKD) and end-stage renal disease (ESRD) Post-obstructive AKI: increased risk for patients with larger stones, bilateral ureteral stones, those with pre-existing kidney disease, and those with a solitary kidney. Although this study suggests the incidence of post-obstructive AKI is rare (1-2%), it is important to think about your patient population and think about how many of them have underlying risk factors. Direct Cellular Toxicity: studies have demonstrated that interaction of calcium oxalate with epithelial cells of the kidney results in mitochondrial dysfunction, release of oxygen free radicals, and subsequently cell death. CKD/ESRD: this review also suggests that nephrolithiasis as an independent risk factor for CKD and ESRD.22 A similar study which compared 21,474 patients with newly diagnosed CKD to matched controls showed that that CKD patients were almost 2 times more likely to have a prior diagnosis of urolithiasis. MD Mkhadar Ali

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