Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Formation of a kidney stone, an organized mass of crystals that grows on the surface of a renal papilla.
Incidence
A.Renal and ureteral stones are a common problem. In the United States, almost 2 million outpatient visits with urolithiasis as primary diagnosis were recorded in the year 2000.
B.The prevalence is increasing from 3.8% (1976–1980) to 8.4% (2007–2010). It coincidentally has increased in concordance with the rising incidence in obesity, insulin resistance, and metabolic syndrome.
C.The condition is more common in males than females. However, the ratio has gone from 1:4 to 1:1.4, as a result of a significant spike in the incidence of the condition in women in the past decades.
D.The average age of onset is 20s to 30s with a second peak in the mid-50s. Up to 16% of men and 8% of women will have at least one symptomatic stone by the age of 70 years.
E.It is more common in whites compared with blacks, Asians, and Hispanics.
F.It is more common in the south-eastern United States and more common in summer because of heat, sunlight exposure, and dehydration, leading to low urine volumes.
G.In stone formers, the rate of recurrence is 30% at 5 years, 50% at 10 years, and 80% at 20 years.
H.In the United States ∼80% of kidney stones are calcium-containing stones, of which 80% are mainly calcium oxalate stones. Less often they are calcium phosphate stones.
Pathogenesis
A.Kidney stones occur as the result of an increased burden of a poorly soluble salt excreted into a volume of urine that is insufficient to dissolve it (supersaturation).
1.In addition to an individual predisposition and/or other factors, there is, especially, lack of inhibitors of crystallization.
2.Supersaturation of poorly soluble salts (i.e., calcium oxalate) in urine is one factor.
B.However, the main factor, especially in calcium-containing stones, is the accumulation of apatite (calcium phosphate) in the medullary interstitium; this may develop in idiopathic hypercalciuria.
1.A stone starts to accumulate in the basement membrane of the thin loop of Henle and grows into the medullary interstitium, to finally form the Randall’s plaque
that will erupt breaking the urothelium of the papilla.
2.This favors the deposition and aggregation of crystals, resulting in the organized stone.
Predisposing Factors
A.Idiopathic hypercalciuria.
B.Obesity, diabetes, and metabolic syndrome: Uric acid stones and calcium oxalate stones.
C.Dehydration, low fluid intake, and low urine volume (summer months, hot and/or dry weather, athletic, or occupational activities).
D.High dietary salt.
E.High oxalate food intake (e.g., spinach, nuts, chocolate, berries, tea, rhubarb, star fruit).
F.High animal protein diet.
G.Protein supplements.
H.Excessive vitamin C supplementation (metabolized to oxalate).
I.Low calcium diet with main meals of the day.
J.Bariatric surgery (gastric bypass).
K.Rapid weight loss/starvation.
L.Hypocitraturia, metabolic acidosis, hypokalemia, or hypomagnesemia.
M.Intestinal malabsorption.
N.Antibiotics (leading to loss of Oxalobacter formigenes, a protecting bacteria of the gut microbiota against excess oxalate absorption).
O.Chronic or recurrent urinary tract infection (UTIs) with urea-splitting organisms such as Proteus, Providencia, or Ureaplasma (struvite stones).
P.Medications: Topiramate, acetazolamide, atazanavir, indinavir, triamterene, sulfadiazine, sulfasalazine, or felbamate.
Q.Systemic diseases: Primary hyperparathyroidism, distal renal tubular acidosis (type 1), sarcoidosis/tuberculosis, medullary sponge kidney, malignancy, intestinal malabsorption (i.e., Crohn’s disease), hyperthyroidism, and so forth.
Subjective Data
A.Common complaints/symptoms.
1.Flank pain (radiates downward and anteriorly to the abdomen, pelvis, and groin/genitals).
2.Nausea and vomiting.
3.Hematuria (gross or microscopic).
4.Stone passage.
B.Common/typical scenario.
1.Fever.
2.Dysuria.
3.Calculous anuria.
4.Interruption of urinary stream.
C.Review of systems.
1.Establish onset and characteristics of the pain.
2.Ask about witnessed stone passage.
3.Ask about stone history.
a.Age when first stone developed.
b.Number of stones.
c.Frequency of stone episodes.
d.Size of stone (passed or still retained).
e.Type of stone (if known).
f.Kidney involved (left, right, or both).
g.Need of urologic intervention (if yes, response to the intervention).
h.UTI associated (yes or no).
4.Inquire about diet, at-risk occupations (e.g., pilots, taxi drivers, teachers, athletes), family history, medications, dietary supplements, medical conditions, previous episodes of urolithiasis, and frequency of UTIs.
Physical Examination
A.The physical examination is most important for ruling out other conditions. Kidney and ureteral stones have no specific manifestations on physical examination.
B.Cerebrovascular accident (CVA) tenderness can be positive in some cases.
Diagnostic Tests
A.Noncontrast CT scan (stone protocol) is the gold standard.
B.Renal ultrasound (inexpensive, safe) is a good diagnostic tool to diagnose urolithiasis and rule out hydronephrosis, especially for frequent stone formers or patient with contraindication for radiation (i.e., pregnancy).
C.Plain radiography of the abdomen shot at 60 kV (kidney–ureter–bladder [KUB]) is useful for the
frequent calcium stone former to reduce the amount of radiation and is more economic.
1.Does not detect non-calcium stones (i.e., uric acid stones).
D.Laboratory analysis should be performed after the first kidney stone episode.
1.Serum electrolytes, including calcium and phosphorus.
2.Blood urea nitrogen (BUN) and creatinine.
3.Uric acid level.
4.In patients with hypercalcemia.
a.Parathyroid hormone (PTH) level.
b.25-OH vitamin D.
c.1,25 dihydroxyvitamin D.
5.A low-serum bicarbonate concentration.
a.Urine pH.
i.6.0 or more: Suggests renal tubular acidosis.
ii.Greater than 8 urine pH or pyuria: Should lead to urine cultures and consideration of struvite stones.
6.Ancillary 24-hour urine collection for stone-risk profile is recommended in these situations.
a.All children with kidney stones.
b.Metabolically active stones (growing in size or in number within 1 year).
c.Frequent stone formers (more than two to three episodes).
d.Non-calcium (e.g., cystine, uric acid) stone formers.
e.Patient in demographic group not typically prone to stone formation (e.g., African Americans).
Differential Diagnosis
A.Pyelonephritis (although in many situations coexist with nephrolithiasis).
B.Peritonitis.
C.In women: Ovarian torsion, ovarian cyst, or ectopic pregnancy.
Evaluation and Management Plan
A.General plan.
1.Pain relief.
a.Patients can be managed at home if they are able to take oral medications and fluids.
b.Combination of nonsteroidal anti-inflammatory drugs (NSAIDs) and opioids is superior than each agent alone (i.e., morphine 5 mg + ketorolac 15 mg).
2.Fluid intake.
a.The mainstay of therapy is to increase the urine volume to more than 2 L per day.
b.Therefore, the patient has to be encouraged to drink around 3 L of fluid per day. Because the risk of stone formation is highest during the night time, patients should be encouraged to drink plenty of fluids in the evening.
3.Sodium intake.
a.Urine sodium excretion augments urine calcium excretion.
b.Hence, the patient should be instructed to limit dietary sodium to 2 g per day.
4.Dietary calcium.
a.It has been demonstrated that an adequate calcium intake in the diet decreases kidney stone incidence. This is likely due to intestinal binding of calcium to oxalate, preventing its absorption.
b.An age- and gender-appropriate calcium diet is therefore recommended. Calcium supplementation outside of meals should be avoided.
B.Specific treatment (for each stone type).
1.Calcium stones.
a.Potassium citrate 30 to 60 mEq/day PO.
i.Would start with 60 mEq/day if 24-hour urinary citrate is less than 150 mg/day.
ii.Titrate dose to a 24-hour urinary citrate 320 to 640 mg/day and a urinary pH 6.0 to 7.0, to inhibit stone formation.
b.Thiazide diuretic: Patients with hypercalciuria (24-hour urinary calcium >250 mg/day).
i.Chlorthalidone 12.5 mg PO daily, or hydrochlorothiazide 12.5 mg PO daily, or indapamide 1.25 mg PO daily.
ii.If the calcium excretion remains elevated in follow-up 24-hour urinary calcium several months after, the thiazide dose should be increased.
c.Dietary oxalate restriction: Patients with hyperoxaluria (24-hour urinary oxalate >25–30 mg/day). Supplement each meal with calcium carbonate 1 to 1.5 g and snack to bind dietary oxalate in the intestine and prevent absorption.
d.Specific therapy for malabsorptive disorder: First-line treatment for enteric hyperoxaluria.
2.Uric acid stones.
a.Potassium citrate: 30 to 60 mEq/day or twice daily orally to dissolve retained uric acid stones.
i.For prevention of new stones: 30 to 60 mEq/day or three times a week titrating urinary pH to greater than 7.0.
ii.Patient use of colorimetric pH-sensitive urine strips: Check the urinary pH 3 to 4 hours after taking potassium citrate.
b.Low purine and low animal protein diet, if in follow-up the 24-hour urine uric acid is still high (>700 mg/day).
i.May need to add allopurinol 100 mg/day PO, increasing weekly to 200 to 300 mg/day.
3.Struvite stones (staghorn calculi).
a.Aggressive medical and surgical treatment, since this can lead to renal failure.
i.Early urologic intervention is advised.
b.Antibiotic therapy, to prevent further stone formation due to urease splitting organisms.
4.Cystine stones.
a.Treatment to decrease cysteine concentration: Water intake as mainstay of therapy.
i.Trying to achieve 3 to 4 L of urine a day.
ii.Goal urine cystine concentration less than 243 mg/L.
b.Low sodium diet 2 g/day.
c.Low animal protein diet.
d.Potassium citrate: Goal urine pH greater than 7.0 (maintained), which is a difficult task.
i.Start 20 mEq TID and titrate up to a pH greater than 7.0.
e.Tiopronin 400 to 1,200 mg/day in three divided doses (comes in 100 mg tablets).
i.Fewer side effects than D-penicillamine, but still can cause the same side effects (i.e., proteinuria, fever, rash, abnormal taste, arthritis, leukopenia, aplastic anemia, and hepatotoxicity).
C.Hospitalization.
1.Stone greater than 5 mm (98% of stones <5 mm will pass spontaneously).
2.Nausea and vomiting; unable to take oral medicine or fluids.
3.Requiring parenteral therapy for pain.
4.Pyelonephritis/UTI.
Follow-Up
A.For adult patients with history of only one calcium-containing kidney stone that passed spontaneously, no special follow-up is required.
B.For frequent stone formers (two to three or more episodes), children, or individuals who form non-calcium stones or rare stone types, they need a follow-up in 4 to 6 months with a 24-hour stone risk analysis to monitor the effect of therapy.