KIDNEY STONES

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• KIDNEY STONES

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• nephrolithiasis (kidney calculi or stones) is
  well-documented common occurrences in the general
  population
• The etiology of this disorder is multifactorial
  and is strongly related to dietary lifestyle
  habits or practices.
• Urinary calculi or stones are the most common
  cause of acute ureteral obstruction.
• The term nephrolithiasis (kidney calculi or
  stones) refers to the entire clinical picture of
  the formation and passage of crystal agglomerates
  called calculi or stones in the urinary tract

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• Activity means
• Formation of new stones
• Enlargement of old stones
• Passage of gravel
• Despite attempted dietary modification
  over a 3 to 6 month period.

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• Nephrocalcinosis calcification of renal papilla
  that if break loose cause colic
• Sludge sufficient uric acid or cystine in the
  urine may plug both ureters with precipitate
• Staghorn calculi struvite, cystine, and uric acid

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Epidemiology

• 31 MF (7 men/ 3 women) Women typically
  excrete more citrate and less calcium than men
• Ethnic Background Stones are rare in Native
  Americans, Africans, American Blacks, and
  Israelis
• 3rd-5th decade most common (70)
• predispositicve diseases (RTA type 1,
  Hyper-parathyroidism, cysteinuria, milk-alkali
  syndrome, sarcoidosis, Crohn's disease)
• Family History produce excess amounts of a
  mucoprotein in the kidney or bladder allowing
  crystallites to be deposited and trapped forming
  calculi or stones
• Climate (mountainous, desert, or tropical)
• Time of year (warmest three months)
• Lifestyle (sedentary)
• Medications protease inhibitors, carbonic
  anhydrase inhibitors

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• 10 of all people will have a kidney stone in
  their lifetime
• 1 in 1,000 adults are hospitalized annually in
  the United States for renal calculi
• 50 of those who develop a renal stone will have
  a recurrence within the next 5-7 years
• Urinary calculi found in 1 of all autopsies

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Types of Renal Calculi

• Calcium Stones
• Calcium Oxalate (60)
• Calcium Phosphate (10)
• Calcium Oxalate and Calcium Phosphate (10)
• Struvite Stones (10-15)
• Uric Acid Stones (5-10)
• Cystine Stones (1-2)

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• Any factor that reduces urinary flow or causes
  obstruction, which results in urinary stasis or
  reduces urine volume through dehydration and
  inadequate fluid intake, increases the risk of
  developing kidney stones.
• Low urinary flow is the most common abnormality,
  and most important factor to correct with kidney
  stones. It is important for health practitioners
  to concentrate on interventions for correcting
  low urinary volume in an effort to prevent
  recurrent stone disease

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Pathophysiology

• Formation requires four key elements
• Supersaturation of urine with solutes
• Relative lack of the inhibitors citrate
  pyrophosphate
• Nucleation
• Stasis or lack of urine flow

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Clinical Presentation

• Symptoms may vary and depend on the location and
  size of the kidney stones or calculi within the
  urinary collecting system. In general, symptoms
  may include acute renal or ureteral colic,
  hematuria (microscopic or gross blood in the
  urine), urinary tract infection, or vague
  abdominal or flank pain. A thorough history and
  physical examination, along with selected
  laboratory and radiologic studies, are essential
  to making the correct diagnosis. Small
  nonobstructing stones or "silent stones" located
  in the calyces of the kidney are sometimes found
  incidentally on x-rays or may be present with
  asymptomatic hematuria. Such stones often pass
  without causing pain or discomfort

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Area of impaction

• UPJ
• where ureter passes over pelvic brim and iliac
  vessels
• UVJ smallest diameter of the urinary tract
• In FM the posterior pelvis ureter is crossed
  anteriorly by the pelvic blood vessels and broad
  ligament

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Consequences of urinary tract obstruction

• Reduced glomerular filtration rate
• Reduced renal blood flow (after initial rise)
• Impaired renal concentrating ability
• Impaired distal tubular function
• Nephrogenic diabetes insipidus
• Renal salt wasting
• Renal tubular acidosis
• Impaired potassium concentration
• Postobstructive diuresis

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Acute urinary tract obstruction

• Functional consequences

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Calcium Stones

• Hereditary Hypercalciuria condition
• Main risk factor for calcium stone development in
  the United States
• Mean value of calcium in urine in excess of
• 300 mg/day (7.5 mmol/day) for males
• 250 mg/day (6.25 mmol/day) for females
• 30-40 patients with calcium stones have
  hypercalciuria

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Struvite Stones

• Triple phosphate or infection stones
• Occur twice as often in women than in men
• Form only with presence of bacteria that have
  urea-splitting enzyme urease
• Proteus mirablis, Kelbsiella, Serratia,
  Mycoplasma, Psuedomonas, Urealyticum
• Alkaline urine promotes struvite calculi
  formation
• Urea-splitting organisms break down urea
• Carbon dioxide and ammonia are produced
• Urine pH increases
• Carbonate levels rise

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Uric Acid Stones

• Uric Acid end product of purine metabolism
• Derived from exogenous sources
• Produced endogenously during cell turnover
• Contributing disease states to uric-acid stones
• Inflammatory bowel disease, lymphoproliferative
  and myeloproliferative disorders due to increased
  cellular breakdown which causes purines to be
  released and so increases uric acid load

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Cystine Stones

• Autosomal recessive trait
• Inborn dysfunction in reabsorption of dibasic
  amino acids like cystine, ornithine, lysine,
  arginine (sometimes seen as COLA) from renal
  tubules
• 1 in 15,000 people in U.S are affected
• Normal cystine excretion lt 20 mg/day
• gt 7.0 urine pH promotes cystine solubility
• Medical Nutrition Therapy increase fluid intake
  gt4 L/day, decrease sodium, may restrict protein
  since methionine is precoursor to cystine
• Standard Medical Practice with medications,
  keep pH alkaline 24 hrs/day

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Preventive therapy

• It is limited to recurrent stone formers, which
  includes patients in whom helical CT on initial
  symptoms presentation shows evidence of more than
  one stone.

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MONITORING

• 24 hour urine collection 4 to 8 weeks after
  recommendation, if negative every year.
• Ultrasonography at one year if negative every 2
  to 4 years thereafter.

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• Calcium Oxalate Stones

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MANAGEMENT

• Lifestyle Change
• Dietary modification
• High fluid intake
• Reduced protein intake
• Limiting sodium intake
• Calcium intake

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Foods and drinks containing oxalate

• beets
• chocolate
• coffee
• cola
• nuts
• rhubarb
• spinach
• strawberries
• tea
• wheat bran

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Drug therapy indicated if the stone disease
remains active

• Activity means
• Formation of new stones
• Enlargement of old stones
• Passage of gravel
• Despite attempted dietary modification
  over a 3 to 6 month period.
  

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MEDICATION

• Thiazide duretics for hypercalciuria
• Allopurinol or potassium citrate for
  hyperuricosuria
• potassium citrate for hypocitraturia
• potassium citrate for type 1 renal tubular
  acidosis

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