1. Clinicians should obtain a single 24-h urine specimen for stone risk factors within 6 months of the initiation of treatment to assess response to dietary and/or medical therapy [Expert Opinion]
2. After the initial follow-up, clinicians should obtain a single 24-h urine specimen annually or with greater frequency, depending on stone activity, to assess patient adherence and metabolic response [Expert Opinion]
3. Clinicians should obtain periodic blood testing to assess for adverse effects in patients on pharmacological therapy [Standard; Evidence Strength Grade: A]
4. Clinicians should obtain a repeat stone analysis, when available, especially in patients not responding to treatment [Expert Opinion]
5. Clinicians should monitor patients with struvite stones for reinfection with urease-producing organisms and utilize strategies to prevent such occurrences [Expert Opinion]
6. Clinicians should periodically obtain follow-up imaging studies to assess for stone growth or new stone formation based on stone activity (plan abdominal imaging, renal ultrasonography, or low dose computed tomography [CT]) [Expert Opinion]
Serum Testing
A basic metabolic panel (including serum glucose, blood urea nitrogen, sodium, potassium, chloride, bicarbonate, creatinine, and calcium) should be obtained in all stone formers. Serum phosphorus and uric acid may also be helpful in the work-up [1, 2]. Serum chemistries may suggest underlying medical conditions associated with stone disease. Hypokalemia and low serum bicarbonate are features of Type 1 renal tubular acidosis. High serum calcium and low serum phosphate would be indicative of primary hyperparathyroidism. Hyperuricemia may suggest a risk of gout [1–3].
A number of medications prescribed for stone prevention are associated with potential adverse effects, some of which can be detected upon follow-up serum testing. Table 13.2 describes common medications used for stone prevention and potential side effects that can be picked up on serum testing. Furthermore thiazide diuretics may uncover patients with primary hyperparathyroidism. Patients with undiagnosed primary hyperparathyroidism may develop hypercalcemia after being started on thiazide therapy [1].
Table 13.2.
Adverse effects of medications used to prevent urolithiasis detected via serum testing.
Medication | Effect on serum testing |
|---|---|
Thiazide diuretics (HCTZ, chlorthalidone, indapamide) | Hypokalemia, hyperglycemia/glucose intolerance, hyperuricemia, increased serum cholesterol [may also lead to hypocitraturia or hyperuricosuria on urinary testing] |
Potassium citrate | Hyperkalemia |
Sodium citrate | Hypernatremia |
Allopurinol | Elevated LFTs |
Tiopronin | Elevated LFTs, Anemia |
Acetohydroxamic acid | Anemia |
A baseline evaluation of kidney function is necessary and should be tracked over the years that the patient has a history of urolithiasis. Though there has been a correlation between a decrease in glomerular filtration rate and kidney stones, the exact etiology of this association has not been well established and may be multi-factorial (caused by recurrent episodes of ureteral obstruction, repeat urologic interventions, or due to stone disease itself as in the case of nephrocalcinosis) [4].
If serum calcium levels are borderline or elevated (>10.0 mg/dL), measurement of intact parathyroid hormone level is recommended to rule out primary hyperparathyroidism as the etiology of stone formation [1, 2]. An ionized serum calcium may be helpful if both serum calcium and PTH are at the high end of the normal values to diagnose primary hyperparathyroidism. Secondary hyperparathyroidism due to vitamin D deficiency would be suspected if PTH is high and serum calcium is low or normal. One would also expect urinary calcium to be low. Measurement of 25-hydroxy-vitamin D would then be indicated (and would be found to be low).
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