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Common Urological Problems

Stone Varieties

  • - General Urology - Common Urological Problems - Urinary Stone Disease
  • Jul 25, 2010
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Tags: | asymptomatic hematuria | calcium | calcium nephrolithiasis | chronic diarrhea |

Calcifications can occur and accumulate in the collecting system,  resulting in nephrolithiasis.  Eighty to eighty-five percent of all urinary stones are calcareous.

Calcium nephrolithiasis is most commonly due to elevated urinary calcium, elevated urinary uric acid, elevated urinary oxalate,  or a decreased level of urinary citrate.

Hypercalciuria is found as a solitary defect in 12%  of patients and in combination with other defects in an additional 18%.  Hyperuricosuria is identified as a solitary defect in 8%  of patients and associated with additional defects in 16%. Elevated urinary oxalate is found as a solitary finding in 5% of patients and as a combined defect in 16%. Finally, decreased urinary citrate is found as an isolated defect in 17% of patients and as a combined defect in an additional 10%.  Approximately one-third of patients undergoing a full metabolic evaluation will find no identifiable metabolic defect.

Symptoms are secondary to obstruction, with resultant pain, infection, nausea and vomiting, and rarely culminate in renal failure. Asymptomatic hematuria or repetitive urinary tract infections recalcitrant to apparently appropriate antibiotics should lead one to suspect a urinary stone. Calcifications within the parenchyma of the kidney, known as nephrocalcinosis,  rarely cause symptoms,  however,  and usually are not amenable to traditional therapies appropriate for urinary stone disease (Figure 16–3). Nephrocalcinosis is frequently encountered with renal tubular acidosis and hyperparathyroidism. Nephrolithiasis and nephrocalcinosis frequently coexist. Most patients with nephrolithiasis, however, do not have obvious nephrocalcinosis.

Nephrocalcinosis may result from a variety of pathologic states. Ectatic collecting tubules, as seen with medullary sponge kidney, are common. This is frequently a bilateral process. Increased calcium absorption from the small bowel is common with sarcoidosis, milk-alkali syndrome, hyperparathyroidism, and excessive vitamin D intake. Disease processes resulting in bony destruction,  including hyperparathyroidism,  osteolytic   lesions,  and   multiple myeloma, are a third mechanism. Finally, dystrophic calcifications forming on necrotic tissue may develop after a renal insult.

Urinary Stone Disease

Urinary Stone Disease

1. Absorptive hypercalciuric nephrolithiasis -
Normal calcium intake averages approximately 900–1000 mg/day.  Approximately one-third is absorbed by the small bowel, and of that portion approximately 150–200 mg is obligatorily excreted in the urine. A large reservoir of calcium remains in the bone. Most dietary calcium is excreted in the stool.  Absorptive hypercalciuria is secondary to increased calcium absorption from the small bowel,  predominantly from the jejunum. This results in an increased load of calcium filtered from the glomerulus. The result is suppression of parathyroid hormone, leading to decreased tubular reabsorption of calcium, culminating in hypercalciuria (>4 mg/kg). This physiologic cascade is in response to the primary defect, an increased absorption of calcium from the small bowel.

image Figure 16–3.  Retrograde pyelogram demonstrating multiple punctate calcifications within the renal parenchyma establishing the diagnosis of nephrocalcinosis.
Renal pelvis and infundibula are free of calculi.

Absorptive hypercalciuria can be subdivided into 3 types. Type I absorptive hypercalciuria is independent of diet and represents 15% of all calcareous calculi. There is an elevated urinary calcium level (>150–200 mg/24 h) even during a calcium-restricted diet. Cellulose phosphate is an effective nonabsorbable exchange resin.  This effectively binds the calcium in the gut,  preventing bowel absorption. Cellulose phosphate has no impact on the calcium transport defect.  Urinary calcium excretion returns to normal values with therapy.

Cellulose phosphate must be taken with meals to be available when calcium is ingested. A typical dose is 10–15 g orally in 3 divided doses and is well tolerated. This therapy is relatively contraindicated in postmenopausal women and in children during their active growth cycles. Inappropriate use may lead to a negative calcium balance and a secondary hyperparathyroid state. As with all stone formers, long-term follow-up is required. Cellulose phosphate may bind other cations besides calcium, including magnesium.  Secondary hyperoxaluria may develop owing to decreased calcium in the gut. See the section on hyperoxaluria for a more detailed discussion.
Hydrochlorothiazides are an alternative treatment for type I absorptive hypercalciuria. Initially there is a reduction in renal excretion of calcium. The increased absorbed calcium is likely deposited in bone.  Eventually the bone reservoir reaches its capacity and the drug becomes ineffective. Hydrochlorothiazides have limited long-term efficacy (approximately 3–5 years). These drugs have no effect on the defective bowel transport system.  Hydrochlorothiazides may be alternated with cellulose phosphate as an effective treatment regimen.

Type II absorptive hypercalciuria is dietary dependent and is a common cause of urinary stone disease. There is no specific medical therapy. Calcium excretion returns to normal on a calcium-restricted diet. Patients should limit their calcium intake to 400–600 mg/day. Type II absorptive hypercalciuria is not as severe as type I.

Type III absorptive hypercalciuria is secondary to a phosphate renal leak and accounts for 5%  of all urinary calculi. Decreased serum phosphate leads to an increase in 1, 25-dihydroxyvitamin D synthesis. The physiologic cascade culminates in an increased absorption of phosphate and calcium from the small bowel and an increased renal excretion of calcium-hence its classification as absorptive hypercalciuria.  Successful treatment replaces bioavailable phosphate.  Orthophosphate (Neutra-Phos)  inhibits vitamin D synthesis and is administered as 250 mg three to four times daily. It is best taken after meals and before bedtime.  Orthophosphates do not alter intestinal calcium absorption.

2.  Resorptive   hypercalciuric   nephrolithiasis-
About half the patients with clinically obvious primary hyperparathyroidism present with nephrolithiasis.  This group represents less than 5–10% of all patients with urinary stones.  Patients with calcium phosphate stones, women with recurrent calcium stones, and those with both nephrocalcinosis and nephrolithiasis should be suspected of having hyperparathyroidism. Hypercalcemia is the most consistent sign of hyperparathyroidism.

Parathyroid hormone results in a cascade of events starting with an increase in urinary phosphorus and a decrease in plasma phosphorus, followed by an increase in plasma calcium and a decrease in urinary calcium.  Its action on the kidney and on the bone is independent of each other.  Ultimately renal damage is secondary to the hypercalcemia.  It limits the concentrating ability of the kidney and impairs the kidney’s ability to acidify urine.

Surgical removal of the offending parathyroid adenoma is the only effective way of treating this disease. Attempts at medical management are futile.

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