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KID NEY STO NES

KID NEY STO NES. 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.

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KID NEY STO NES

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  1. KIDNEYSTONES

  2. 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

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

  4. 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

  5. Epidemiology • 3:1 M:F (~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

  6. 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

  7. 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%)

  8. 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

  9. 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

  10. 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

  11. 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

  12. 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

  13. baseline Hours Acute urinary tract obstruction Functional consequences

  14. 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

  15. 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

  16. 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

  17. 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: < 20 mg/day • > 7.0 urine pH promotes cystine solubility • Medical Nutrition Therapy: increase fluid intake >4 L/day, decrease sodium, may restrict protein since methionine is precoursor to cystine • Standard Medical Practice: with medications, keep pH alkaline 24 hrs/day

  18. 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.

  19. 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.

  20. Calcium Oxalate Stones

  21. MANAGEMENT Lifestyle Change Dietary modification High fluid intake Reduced protein intake Limiting sodium intake Calcium intake

  22. Foods and drinks containing oxalate beets chocolate coffee cola nuts rhubarb spinach strawberries tea wheat bran

  23. 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.

  24. 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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