14. Renal Stone Disease

Etiology

Supersaturation of urine with the stone components. Solubility is affected by urine pH, urine volume and total solute excretion, which can be modified with medications and diet. 

Risk Factors 

  • Male sex, obesity, family history, previous history of nephrolithiasis, hypertension.
  • 4:1 male predominance. Initial presentation in 3rd and 4th decade. Lifetime prevalence 3-5% and about ½ will have recurrent stone disease. 

Types of Stones

  • Calcium oxalate: predisposed by elevated urinary calcium excretion, hypocitraturia and decreased urine volume. Classically seen in patients with inflammatory bowel disease or short gut syndrome (increased GI oxalate absorption due to increased intestinal permeability and enteric calcium binding luminal fatty acids instead of luminal oxalate). Treat hypercalciuric patients with a thiazide diuretic and encourage hydration.
  • Calcium phosphate: predisposed by elevated urine pH. Classically seen in RTAs.
  • Struvite: also called triple phosphate, or magnesium ammonium phosphate stones. Caused by urea-splitting bacteria (Proteus, Klebsiella, Pseudomonas). Associated with foreign bodies and neurogenic bladder. Often present as staghorn calculi in the renal pelvis. Treatment often requires ESWL or surgery.
  • Uric acid: radiolucent stones that form in acidic urine. Patients with hyperuricosuria are more predisposed to calcium stones by reducing solubility of CaOx. Low urine pH reduces uric acid solubility leading to uric acid stones. Treat with potassium citrate (to alkalinize urine) or allopurinol.
  • Cystine: rare autosomal recessive disorder.
  • Insoluble drugs: rarely, indinavir, triamterene, acyclovir and ephedrine can form stones. 

Evaluation

  • History: sudden onset, colicky, flank pain with radiation to groin. Usually severe and often with nausea and vomiting. Typical patient is constantly moving to find a comfortable position, though the pain usually isn’t affected by position. Localization of pain evolves as the stone migrates: at the ureteropelvic junction flank pain predominates, whereas at the ureterovesicular junction the pain radiates to genitalia with other voiding symptoms (urgency, frequency).
  • For flank pain with hematuria, other differential diagnoses include UTI, urinary tract tumor, renal emboli, renal papillary necrosis, and dissecting AAA with renal artery involvement. 
  • Urinalysis: may show hematuria (90% sensitive), signs of infection, and crystals that can allow for a presumptive identification of stone type. Urine pH may provide evidence of renal tubular acidosis or infection by urea-splitting bacteria (raises pH).
  • Imaging: gold standard is a non-con helical CT with stone protocol. However, strategies that start with initial diagnostic renal ultrasound may reduce radiation exposure.

Management

  • Indications for hospitalization: intractable pain (use NSAIDs like IV ketorolac if no concomitant AKI or opioids), intractable vomiting (need volume repletion, though volume repletion isn’t shown to help with stone passage), severe UTI or sepsis (ABX, IVF), complete obstruction (need ABX, emergent urologic intervention vs. IR for percutaneous nephrostomy tubes).
  • Stone removal: depends on size. 98% stones <5mm pass spontaneously, can do watchful waiting and pain control. However, stones >7-8mm have <20% chance of spontaneous passage and may need urological intervention. Start tamsulosin to help with passing stone if >5mm but <10mm.
  • Metabolic workup: rule out hyperparathyroidism, distal RTA (alkalinizes urine), hyperoxaluria, excess vitamin D, sarcoidosis. Collect 24 urine for metabolic analysis if nephrolithiasis is recurrent or in the following populations: elderly, African-Americans, patients with gout, chronic diarrhea, osteoporosis, nephrocalcinosis, uric acid stones, struvite stones, or cystine stones. Patients should strain urine to allow for biochemical analysis of stone.

 

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