9/18- Obstruction, Infection, and Stones Flashcards
What are some signs/symptoms associated with obstruction?
- Decreased urine output
- Flank pain
- Renal colic/hematuria if associated with stone
- Hesitancy
- Dribbling
- Frequency, nocturia
- Recurrent UTIs (esp in men); PVR>50mL associated with 3-fold increase
What are some anatomical features of hydronephrosis (grossly)?
- Very thin renal cortex with damaged glomeruli
- Blunted pyramids
- Dilated renal pelvic
- Dilated calices
What are some anatomical features of hydronephrosis (ultrasound)?
- Dilation of renal pelvis and calyces In pic, left is normal
What is this ultrasound showing?
Mega-ureter
- Hydronephrosis?
What is this CT scan showing?
Left: kidney very large; swollen
Right: normal
When might you have obstruction with no dilation?
- Hypovolemia
- Retroperitoneal fibrosis
What may cause neurogenic bladder?
- Stroke/TBI/Alzheimer’s
- Spinal cord injury, MS, GBS, myelitis
- Autonomic neuropathies/DM
- Post-natal (spinal block) and narcotics
What can cause physiologic hydronephrosis?
- Pregnancy: usually on right side
- Renal allograft
What can cause urinary tract obstruction (common)?
Kids: most are congenital
Adults are BPH or stones
- Women, think mass/malignancy unless proven otherwise!
What is a risk of urinary tract obstruction?
Urinary stasis -> infections that can spread to renal parenchyma (pyelonephritis) and urosepsis
T/F: anuria is essential to the diagnosis of obstruction?
False
- Partial bostruction can -> polyuria, tubular damage (salt wasting) and fluid debt may result from accumulated fluid
What is the triophasic pattern of UTO?
Triphasic pattern of renal blood flow and ureteral pressure changes
1. GFR declines; RBF increases
- GFR = Kf(Pgc - Pt - pi gc) because of Pt and collecting system pressure
- RBF increases to counterbalance Pt in attempt to prserve GFR (NO, PGE)
2. P elevated but RBF begins decline next 3-4 hrs (Ang II, TXA2, Endothelin)
3. Further decline in RBF, then decrease in Pt and collecting system pressure also occurs (stabilizes) 5 hrs after obstruction
What are the early and chronic pathologic findings of UTO?
T/F: Caliectasis can persist for weeks after decompression of acute obstruction
True; caliectasis can persist for weeks as renal function improves
- CKD (thinning cortex)
How can you treat kidney stones?
- Hydration
- Ureteral dilators (e.g. Flomax)
- Urologic intervention
How can you treat RCC or bladder tumor?
Percutaneous stents
How can you treat urethral obstruction?
- Catheterization
- Cystostomy
What is the prognosis in pts with UTO?
- Complete recovery usually occurs after 1 wk of obstruction
- Minimal recovery occurs after 6 wks of obstruction
What are the long term consequences of UTO?
- If obstruction >12hr, changes in collecting duct function can be dilated/hemorrhage zones; these alterations result in decreased responsiveness to ADH (can mimic nephrogenic DI)
- Renal tubular acidosis; inability for kidneys to acidify urine, because hydrogen transporters are damaged
What is nephrolithiasis?
Kidney stones
- Common
- Easy to evaluate
- Treatable
- Preventable
Are kidney stones more common in men or women? Other epidemiology?
Men (12%, 6% women)
- White > black
- Very common in Middle Easterners
- Bimodal in women (peaks at 35 and 55 yrs)
What is the most common kidney stone composition?
Calcium oxalate
What are characteristics of Ca phosphate stones?
- Radiopaque
- Associated with hypercalciuria (50% will end up idiopathic)
List stone composition possibilities
- Calcium oxalate (no. 1)
- Calcium phosphate
- Struvite
- Uric acid
What are struvite stones?
Aka infection stones
- Bacteria liberate large amts of ammonia from urine urea, raising pH and combining with Mg/P to form mineral (struvite)
- Alkaline pH
- Urinary debris and crystal niduses
Stones composed of: Mg, Ca, ammonium, phosphate, carbonate (struvite)
- Radiopaque!
- Difficult or impossible to eliminate stones: staghorn calculi (cast of pelvicocalyceal system)
What are uric acid stones?
- 2-5% of stones
- Potentiates calcium stone formation
- Uric acid has 2 dissociable protons…
- Consider high cell turnover (e.g. leukemia, myeloproliferative d/o)
- Remember: urate stones are radiotranslucent!
What causes cystinuria?
Autosomal recessive disorder
- Cystine, ornithine, arginine, lysine not reabsorbed in urine
- Cystine transport may be defective in gut and/or nephron
Cystine is a poorly soluble AA
Suspicion:
- Young age
- Family history
- Hexagonal crystals
What can cause drug stones?
- Acyclovir
- HAART (e.g. indinavir, atazanavir)
What cause the Melamine milk crisis?
- Infant milk supplemented with Melamine to raise protein content
- 6 deaths
What conditions favor stone formation?
- Slow urine flow
- High solute concentration
Results in supersaturation of the urine with solutes that tend to crystallize and later form stones
What is nucleation? How does it occur?
Appearance of solid-phase nucleus in a region that had previously had no solid phase
- Hydroxyapatite formation involving renal papillae; Randal’s plaques; serve as nidus for crystallization/extension for Ca containing stones
- Typically starts in basement membrane of thin limbs; in thin LH, slow flow, hyperosmotic mucopolysaccharide matrix, electrostatically charged ionic sites -> ripe template to begin crystallization
What can predispose someone to stones (broadly)?
Decreased inhibitor substances in the urine that would otherwise prevent supersaturation and crystalline aggregation
What are some inhibitors of urinary crystallization?
- Multivalent metallic cations (Mg)
- Small organic (citrate)
- Inorganic anions (Pyrophosphate)
- Macromolecules ranging in size from 10kd
- 100 kd (e.g. Tamm-Horsfall protein) Citrate and Mg are the most significant inhibitors
- Citrate is the most important physiologic inhibitor (shown to increase Ca solubility and coat crystals and prevent growth and aggregation)
What can cause idiopathic hypercalciuria?
- Absorptive: excessive Ca absorbed from GIT
- Renal leak: impaired tubular Ca reabsorption
- Renal phosphaturia: renal Pi losses which causes increased GI reabsorption of Ca and hypercalciuria
What can cause secondary hypercalciuria?
Elevated serum Ca
- Sarcoidosis, TB, other granulomatous diseases
- Malignancy (Lymphoma, bone mets, myeloma, others)
- Paget’s disease of bone
- Immobilization
Endocrine
- Hyper PTH, hyperthyroid, Cushing’s syndrome
Medications
- Loop diuretics, Vit D supp
Renal tubular acidosis
Medullary sponge kidney
Does calcium oxalate inhibit or promote stone formation?
Oxalate potentiates Ca stone formation
What can contribute to high levels of Ca oxalate?
- GI absorption increased with low Ca and Mg diets ( Low GI calcium increases oxalate absorption)
- Malabsorption syndromes (e.g., bacterial overgrowth, short bowel, pancreatitis, IBD, surgical procedure, blind loop syndromes, celiac dz …etc).
—- Increased fatty acid in intestine -> Ca–salts-fatty acids -> Ca not available to bind oxalate -> increased Ox absorption.
- Disordered Ox metabolism: pyridoxine (Vit B6) deficiency, primary hyperoxaluria
How do hypo-citraturia and magnesuria affect stone formation?
- Ca-citrate is more soluble than other Ca compounds, thus Ca available for crystallization is decreased
—- Use K-citrate to increase urinary citrate
—- K increases urinary citrate
- Mg binds oxalate in soluble compound, removing it from crystallizing with Ca
How does bariatric surgery affect stone formaton?
(Roux-en-Y gastric bypass (RYGB) or small-pouch Gastric bypass)
- Risk for stones/renal failure (oxalate nephropathy) equal to that of a patient with primary oxaluria
(Gastric banding not associated with risk of nephrolithiasis)
What is the ultimate factor for stone formation?
Concentration of the solute
- Therefore, reduced urine volume will amplify the saturation of all solutes and raise risk of stone
What to suspect in history of someone with stones?
- History previous stones, frequent urinary infection, hyperparathyroidism, sarcoidosis, RTA, malignancy
- Strenuous exercise during summer
- Medication and diet histories
- Family history of stone disease
- Chronic Foley, stent, other instrumentation
Different presentations of kidney stones?
- Attached to papilla: hematuria but not significant pain
- Lodged stones; sever flank/back pain with radiation into groin
- Nausea, vomiting, urinary frequency, gross hematuria
Common places kidney stones may lodge?
- Ureteropelvic junction (10.6%)
- Proximal ureter (23.4%)
- Where ureter crosses anterior iliac vessels (1.1%)
- Distal ureter (4.3%)
- Ureverovesical junction (60.6%)
What is important in the acute evaluation of kidney stones?
- Hx = most important
- Serum: basic metabolic profile
Urine:
- UA (hematuria), culture and sensitivity
- DO NOT perform urinary profile during acute stone work-up (not representative)
- Stone analysis if one available
T/F: You may not see a stone that is already in the ureter on renal ultrasound?
True
What is the imaging method of choice for kidney stones?
CT scan- images kidney and ureter
Pros and cons of IVP?
- Widely available
- Shows urinary tract very well
- Disadvantage: requires IV contrast
How to treat acute stone?
- Confirm diagnosis, R/O renal failure and sepsis
- Pain relief; IVF; +/-alpha blocker; +/- ureteroscopy/ureteral stent
- Follow-up to confirm stone passed
- Decide on level of evaluation
—- If first stone, no other disease or family history, screen patient with routine lab
—- If multiple stones, family history, or renal failure, more detailed workup
What is ESWL?
Estracorporeal shock wave lithotripsy (ESWL)
- Noninvasive
- Effective for stones under 1 cm, especially distal ureteral stones or lower pole stones
What is URS?
Ureteroscopy
- Invasive
- Effective for all stones including > 1 cm
What are the odds of recurrence of kidney stones without preventative therapy?
- 20%: 1-3 yrs
- 40-50% by 5 yrs
- 50-60% by 10 yrs
- 75% by 20-30 yrs
What are methods to prevent stones?
- Drink 3L/d to ensure at least 2 L urine/d (don’t guide therapy by urine color)
- Juice does NOT reduce risk (grapefruit juice increased risk)
- Limit salt intake under 3 g/d (increased urinary elimination of salt -> more Ca in urinary filtrate; low Na increases proximal Na reabsorption which increases renal tubular Ca reabsorption)
- Limit intake of nuts if due to hyperoxaluria
- Hypokalemia decreases urinary citrate
- Higher K intake has been inversely associated with new stone formation in men/older but not younger women
- Decrease animal protein (associated with new stone formation in men but not women)
- Less vitamin C (supplement increases urine oxalate)
- More Mg: complexes with oxalate (decreasing in urine) and may decrease oxalate absorption in gut
What is some pharmacologic intervention for stones?
- Thiazides: decreases urinary Ca
- Allopurinol for hyperuricosuria
- Pyridoxine for primary hyperoxalauria
- Potassium Citrate for hypocitrituria/ acidotic states or low urine pH
- Abx therapy for urea-splitting organisms
- Cystine-binding drugs increase solubility 50-200x: D-penicillamine, 2-mercaptopropionylglycine, captopril
- ?Probiotic: O. formigenes (gut flora) is associated with 70% reduction in risk for recurrent stones
Concepts to remember:
- Obstructive nephropathy frequent and causes can vary widely (have suspicion)
- Triphasic patter of UTO
- Early relief of obstruction results in improved prognosis
- Remember stone types and crystal appearance
- Strong genetic component (cysteine, Ca stones, but also diet/co-morbidity (e.g., uric acid)
- Acute management
- Chronic prevention (stone prevention)
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