eMedicine Specialties > Urology > Stones

Hypocitraturia: Follow-up

Author: George Bennett Stackhouse IV, MD, Clinical Fellow in Endourology, Urology, University of California, San Francisco
Coauthor(s): Howard H Woo, MD, Consulting Staff, Clinical Instructor, Department of Urology, Ochsner Urology Institute
Contributor Information and Disclosures

Updated: Jun 16, 2006

Follow-up

Further Inpatient Care

  • When necessary, inpatient care should be directed at only the stone disease. Treatment of underlying hypocitraturia is best accomplished on an outpatient basis after convalescence. Diet and medication should be modified in an atmosphere as close as possible to the patient's normal environment.

Further Outpatient Care

  • The objective of treatment with Urocit-K or Polycitra-K is to provide potassium citrate in sufficient dosage to restore normal urinary citrate (ie, >320 mg/d and as close to the normal mean of 640 mg/d as possible) and to increase urinary pH to a level of 6.0-7.0. Urinary citrate and/or urinary pH measurements should be evaluated every 4 months. Those results should be used to determine the adequacy of the initial dosage and to evaluate the effectiveness of any dosage change. Note that doses of Urocit-K greater than 100 mEq/d have not been studied and should be avoided when possible. Obviously, risk of hyperkalemia is increased when these higher dosages are used, so serum potassium levels should be monitored as well, particularly in cases of renal failure. The pH change after institution of potassium citrate therapy generally is small, although reduced doses may be required, with frequent pH monitoring, to maintain the pH below 7-7.2. At pH levels above 7.2, the risk of calcium phosphate crystallization increases significantly. Calcium phosphate can coat an otherwise dissolvable uric acid stone and prevent it from dissolving, so avoiding overalkalinization when trying to dissolve pure uric acid calculi is particularly important.
  • Initial visit
    • A careful history is taken, and minimum diagnostic tests are conducted.
    • History: Secondary causes include dietary aberrations and stone-provoking drugs. The patient's interest and motivation to follow a course of preventive therapy should be assessed.
    • Minimum diagnostic tests
      • Abdominal radiograph of the KUB
      • Urinary stone/sediment analysis
      • Serum calcium, potassium, electrolytes, creatinine, and uric acid levels
      • Urine analysis and culture
  • A 24-hour urinary stone risk profile on the patient's customary diet
  • Identification of abnormal dietary risk factors
  • Short-term dietary modification
  • Repeat 24-hour profile after short-term dietary modifications.
  • Identification of abnormal environmental and metabolic risks factors
  • Long-term dietary modification with the addition of appropriate supplements and medications, if necessary.

Inpatient & Outpatient Medications

  • Severe hypocitraturia ( <100 mg/d)
    • Chronic diarrheal states - Liquid formulation of potassium citrate
    • Complete distal RTA - Potassium citrate 20-40 mEq PO 2-4 times daily as needed to optimize urinary citrate excretion
    • Infection stones (magnesium and ammonium phosphate or carbonate apatite) - Potassium citrate, antibiotics, stone removal (Potassium citrate should be used cautiously in these situations because alkalinization will increase struvite [infection] stone formation.)
  • Mild-to-moderate hypocitraturia (100-320 mg/d)
    • Dietary causes - Dietary restriction of animal protein and supplemental potassium citrate (initial dose 20 mEq PO bid-tid) is recommended therapy. The dose is adjusted based on urinary pH and citrate levels obtained at 2-3 months of treatment. Once stabilized, repeat testing can be performed at 4- to 6-month intervals and then yearly if stable. Performing a complete, 24-hour urine metabolic screening that includes serum potassium, as well as urinary volume, calcium, uric acid, oxalate, phosphate, sodium, and magnesium in addition to citrate, is important. New problems may develop as diets are adjusted. An adequate fluid volume needs to be maintained even if this means dilution of the citrate concentration. When this occurs, appropriate adjustment of the potassium citrate dosage should be achieved to ensure an optimal concentration of roughly 300 mg of citrate per liter.
    • Incomplete RTA - Potassium citrate supplementation as appropriate
  • Hypokalemia of thiazide treatment – Administer potassium citrate and stop or replace thiazide if possible. When initiating long-term thiazide therapy for hypercalciuria, a potassium citrate supplement often is recommended, even if urinary citrate levels initially are normal.
  • Low-normal urinary citrate level (320-400 mg/d) – Administer potassium citrate (10 mEq PO bid-tid). Consider optimizing 24-hour citrate to 600 mg per 24 hours.

Deterrence/Prevention

  • Adequate amount of hydration to maintain 1.5-2 L or more of urine output per day is a well-accepted stone prevention measure.

Complications

  • Hyperkalemia
  • Abdominal discomfort
  • Vomiting
  • Diarrhea
  • Peptic ulcer disease
  • Formation of urinary stones
  • Meta-analysis shows that up to 48% of patients in long-term studies discontinue oral potassium citrate therapy because of side effects.

Prognosis

  • Approximately 80-90% of patients with hypocitraturia are treated successfully with potassium citrate to raise their urine citrate levels. This reduces the risk of recurrent stone formation.
  • Barcelo and colleagues randomized hypocitraturic stone formers to potassium citrate (30-60 mEq/d, with an average of 45 mEq qd) or placebo for 3 years. Thirty-eight patients completed 3 years of study, 18 in the treatment arm and 20 in the placebo group. Among treated patients, 72% had no further stone formation, compared to 20% in the placebo group. All patients in the treatment group had a decline in their individual stone formation rate.
  • Pak showed remission rates after potassium citrate therapy of 67% (in patients with chronic diarrheal syndromes) to 92% (in those with idiopathic hypocitraturia); all patients showed a reduction in their rate of stone formation.

Patient Education

  • Diet and behavioral modification
  • Risks and benefits of treatment with potassium citrate
  • For excellent patient education resources, visit eMedicine's Kidneys and Urinary System Center. Also, see eMedicine's patient education article Kidney Stones.

Miscellaneous

Medicolegal Pitfalls

  • See Complications and avoid these undesirable problems in clinical practice.
  • Potassium-containing medications should be used with caution in patients with renal insufficiency or in those receiving potassium-sparing diuretics.
  • Citrate therapy may be counterproductive in patients with infection stones.

Special Concerns

  • Potassium-magnesium-citrate has been investigated and may be more effective than potassium citrate in the prevention of stones because it not only increases urinary citrate but also urinary magnesium, which is another well-known inhibitor of stone formation. It is available over-the-counter and on the Internet but has not yet been widely embraced by the urologic community.
 
Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous coauthor Beng Jit Tan, MD, PhD, to the development and writing of this article.



More on Hypocitraturia

Overview: Hypocitraturia
Differential Diagnoses & Workup: Hypocitraturia
Treatment & Medication: Hypocitraturia
Follow-up: Hypocitraturia
References

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Further Reading

Keywords

citrate, citric acid, nephrolithiasis, calcium nephrolithiasis, calcium oxalate, calcium phosphate, alkalinization, uric acid, potassium citrate

Contributor Information and Disclosures

Author

George Bennett Stackhouse IV, MD, Clinical Fellow in Endourology, Urology, University of California, San Francisco
George Bennett Stackhouse IV, MD is a member of the following medical societies: Alpha Omega Alpha and Phi Beta Kappa
Disclosure: Nothing to disclose.

Coauthor(s)

Howard H Woo, MD, Consulting Staff, Clinical Instructor, Department of Urology, Ochsner Urology Institute
Howard H Woo, MD is a member of the following medical societies: American Urological Association
Disclosure: Nothing to disclose.

Medical Editor

Leonard Gabriel Gomella, MD, FACS, Director of Urologic Oncology, Bernard W Godwin Associate Professor of Prostate Cancer, Department of Urology, Kimmel Cancer Center, Thomas Jefferson University
Leonard Gabriel Gomella, MD, FACS is a member of the following medical societies: American Association for Cancer Research, American College of Surgeons, American Medical Association, American Society for Laser Medicine and Surgery, American Urological Association, Sigma Xi, Society for Basic Urologic Research, Society of University Urologists, and Society of Urologic Oncology
Disclosure: Nothing to disclose.

Pharmacy Editor

Francisco Talavera, PharmD, PhD, Senior Pharmacy Editor, eMedicine
Disclosure: Nothing to disclose.

CME Editor

J Stuart Wolf, Jr, MD, FACS, David A Bloom Professor of Urology, Director, Division of Minimally Invasive Urology, Department of Urology, University of Michigan Medical Center
J Stuart Wolf, Jr, MD, FACS is a member of the following medical societies: American College of Surgeons, American Medical Association, American Urological Association, Catholic Medical Association, Endourological Society, Society for Urology and Engineering, Society of Laparoendoscopic Surgeons, and Society of University Urologists
Disclosure: Terumo Corporation Consulting fee Consulting; Omeros Corporation Consulting fee Consulting

Chief Editor

Stephen W Leslie, MD, FACS, Founder and Medical Director of the Lorain Kidney Stone Research Center, Clinical Assistant Professor, Department of Urology, Medical College of Ohio
Stephen W Leslie, MD, FACS is a member of the following medical societies: American College of Surgeons, American Urological Association, National Kidney Foundation, and Ohio State Medical Association
Disclosure: Nothing to disclose.

 
 
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