Hydronephrosis Flashcards

1
Q

What is the blood supply of the kidneys?

A
  • The renal artery supplies blood to the kidney and proximal ureter, as well as small branches off the gonadal artery and aorta
  • The middle ureter is fed by blood vessels from the common iliac artery, internal iliac, superior vesical, middle rectal, and inferior vesical arteries
  • Proximal to the iliac artery, the blood supply comes medially distal to the iliac artery; it comes laterally
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2
Q

What are the significant regions of the ureter when it comes to obstruction?

A
  • It is important to understand the blood supply of the ureter when contemplating surgery on it
  • The ureter has a variable diameter of approximately 5-10mm but has 3 distinct areas of narrowing:
    • the ureteral pelvic junction (2-3mm)
    • the region over the iliac vessels (4mm)
    • and the ureteral vesical junction (2-4mm)
  • Stones, which typically form in the kidney, tend to hang up these areas of narrowing, causing obstruction and renal colic
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3
Q

What are the three major categories of acute renal failure?

A
  • Acute renal failure can be sub-categorized into 3 groups: prerenal, renal, and postrenal
  • This lecture will deal with postrenal obstruction
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4
Q

Define the following terms: hydronephrosis, obstructive uropathy, and obstructive nephropathy.

A
  • Hydronephrosis: is a descriptive term referring to dilatation of the renal pelvis and calyces
  • Obstructive Uropathy: is structural impedence to the flow of urine anywhere along the urinary tract
  • Obstructive Nephropathy: refers to damage of the renal parenchyma resulting from obstruction of urine flow anywhere along the urinary tract
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5
Q

What is the presentation of acute renal obstruction?

A
  • Patients with acute obstruction typically present with:
    • flank pain
    • lower abdominal pain
    • groin pain
    • penile or testicular pain
    • inner thigh pain
    • nausea
    • vomiting
    • when infection is present:
      • fevers and chills
  • Serum studies may show azotemia and hyperkalemia
  • Hematuria, proteinuria, and pyuria may be present in the urine. With bilateral obstruction patients are anuric.
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6
Q

What are the phases of obstruction?

A
  • Acute obstruction has 3 phases:
    • Phase I: renal blood flow and ureteral pressure rise (1-1.5 hours)
    • Phase II: decreased renal blood flow and increased ureteral pressure (1.5-5 hours)
    • Phase III: decreased renal blood flow, decreased ureteral pressure (greater than 5 hours)
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7
Q

Describe the process of recovery after kidney damage from obstruction.

A
  • Damage to the kidney occurs gradually over a period of 6 weeks
  • Studies in dogs have shown that with unilateral ureteral obstruction of 7 days, full recovery is possible within 2 weeks
  • Fourteen days of unilateral ureteral obstruction results in permanent decline in renal function to 70% of control levels with 3-6 months necessary for recovery time
  • After 4 weeks of unilateral ureteral obstruction, some recovery is possible
  • After 6 weeks, no recovery is possible
    • This is an important point when managing ureteral stones as patients can safely be followed for up to a week, allowing them time to spontaneously pass the stones
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8
Q

What are the gross and histologic findings of an obstructed kidney?

A
  • Grossly obstructed kidneys become hydronephrotic with compression of the papillae, caliceal blunting, and thinning of the parenchyma
  • Histologically, there is dilatation of the tubules and glomerular hyalinization
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9
Q

What is the presentation of chronic renal obstruction?

A
  • Patients with chronic obstruction typically present with:
    • weight gain
    • edema
    • malaise
    • uremia (resulting in mental status changes, tremors and bleeding)
    • and typically in males
    • may have a weak or intermittent stream
    • overflow incontinence
    • polyuria secondary to a poor concentrating ability
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10
Q

What are the diagnostic tests for renal obstruction?

A
  • Obstruction is typically diagnosed by a variety of radiographic studies:
    • Intervenous urogram / Pyelogram (IVU or IVP), which typically shows a delayed nephrogram, delayed pyelogram, hydronephrosis, columning, and in high-grade obstruction, forniceal rupture
    • Ultrasonography shows dilated collecting system and echoic central areas in the normally eugenic renal sinus with parenchymal thinning
    • Computerized tomography (typically shows findings similar to ultrasonography)
    • Diuretic renography shows an elevated T1 half (clearance of tracer after Lasix) with less than 10 minutes considered normal, 10-20 min. elevated, greater than 20 min. indicative of obstruction
    • Whitaker test is the gold standard for determining obstruction. Percutaneous infusion of saline in contrast into the renal pelvis at 10ml/minute shows a pressure gradient typically of less than 15cm of water. If the pressure gradient is greater than 22cm of water, this is indicative of obstruction
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11
Q

What is post obstructive diuresis?

A
  • Post obstructive diuresis refers to polyuria after release of bilateral obstruction
  • It is the normal physiologic release of urea, sodium and water
  • In pathologic conditions, there is impaired concentrating ability and sodium resorption
  • If urine output is >200ml/hour for 2 hours, or the urine osmolality is low, or the patient is unable to drink, urine should be replaced at a rate of one half cc of D5.45 normal saline per cc of urine
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12
Q

What is the presentation of a combination of obstruction and infection? What is the treatment?

A
  • The combination of obstruction and infection can be deadly
  • Typically, these patients have flank pain, fevers, chills, leukocytosis, pyuria and bacteri urea
  • Urine enters the blood stream via pyelolymphatic and pyelovenous back flow
  • Forniceal rupture may lead to a perinephric abscess, typically contained within Gerota’s fascia
  • Patients with obstruction and infection should immediately have their blood and urine cultured
  • Broad-spectrum intervenous antibiotics should be started and the obstructed kidney or bladder should be drained with percutaneous nephrostomy tubes, ureteral stents, or urethral catheters
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13
Q

What is the presentation and etiology of urolithiasis?

A
  • Urolithiasis occurs with supersaturation, crystallization and aggregation
  • When the solubility product (Ksp) is reached, crystallization occurs
  • More important is the formation product as urine is metastable with respect to calcium oxalate due to factors such as inhibitors, matrix, and nucleation
  • Intrinsic factors causing urolithiasis are hereditary factors, age, and sex
  • Extrinsic factors include geography, water intake, diet and occupation
  • The etiology of stones in 95% of cases can be determined by a metabolic stone evaluation, which includes two 24-hour urine collections and blood tests
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14
Q

What are the imaging findings of urolithiasis?

A
  • 75% of stones are formed of calcium oxalate and calcium phosphate
    • These tend to be radiopaque in nature and typically are caused from hypercalciuria, hyperoxaluria and hypocitraturia
  • Magnesium ammonium phosphate (struvite) stones are the result of infection with urea-splitting bacteria and compose 8% of kidney stones
    • These stones are radiopaque
  • Uric acid stones occur in 6% of the population
    • They are radiolucent and form in acid (pH5) urine
    • Cystine stones are rare (2% of stones) and are secondary to homocystinuria
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15
Q

What are the different types of stones and what are the diagnostic findings and predisposing factors?

A
  • Calcium oxalate with or without calcium phosphate
    • 75%
    • Opaque
      • Hypercalciuria
      • Hyperuricosuria
  • Pure calcium phosphate
    • 9%
    • Opaque
      • Renal tubular acidosis
      • Medications: Diamox, Calcium, Vitamin D
  • Magnesium ammonium phosphate (struvite)
    • 8
    • Opaque
      • Infection with urea-splitting bacteria
  • Uric acid
    • 6%
    • Lucent
      • Hyperuricosuria
      • ​Acid urine
      • ​Low urine volume
  • Cystine
    • 2%
    • Opaque
      • Cystinuria
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16
Q

What is the definition of hypercalcuria, and what are the three major causes?

A
  • Most stone formation is due to underlying metabolic abnormalities. Hypercalciuria refers to elevated levels of calcium in the urine (greater than 250mg/24 hours). There are 3 causes of hypercalciuria:
    • Resorptive hypercalciuria occurs when calcium is resorbed from bones
      • This condition typically occurs with hyperparathyroidism and patients have elevated serum calcium levels
      • The treatment for this condition is parathyroidectomy
    • Absorptive hypercalciuria is the most common cause of hypercalciuria and occurs from increased absorption of calcium in the gut
      • This is typically treated with thiazide diuretics
    • Renal leak hypercalciuria is due to excess leakage of calcium from the kidney into the urine and is treated with thiazide diuretics
17
Q

What is the definition of hyperoxaluria?

A
  • (greater than 40mg/24 hours) refers to too much oxalate in the urine
  • In some rare cases, it can be caused by a primary liver disease (oxalosis), but is more commonly due to increased absorption in the bowel
18
Q

What is the definition of hypocituria?

A
  • (less than 320ml/24 hours) refers to low citrate levels in the urine
  • Citrate inhibits kidney stone formation and can be treated with diet, dietary modifications (lemonade), or potassium citrate tablets
19
Q

What is the definition of hyperuricosuria?

A
  • (greater than 600ml/24 hours) refers to excessive uric acid levels in the urine
  • This can be seen in gout or in patients with excessive purine (meat, fish, etc.) intake
20
Q

What is the definition of struvite stones?

A
  • Caused by urease producing bacteria (proteus, klebsiella, pseudomonas, staphylococcus, etc.)
  • Urease producing bacteria use urease, an enzyme, to supply their demand for nitrogen, which they obtain for the urine
  • Urea represents the principal excretory nitrogenous product in the urine
  • Bacteria split urea with urease to produce ammonia (NH3)
  • Calcium, magnesium, and phosphate, which are normally present in the urine combine with ammonium (NH4+) at pH greater than 7.2 to form struvite stones (Magnesium ammonium phosphate stones)
21
Q

What is the definition of cystinuria?

A
  • Refers to the inborn error of transport of dibasic amino acids:
    • cystine
    • ornithine
    • lysine
    • arginine
  • Excessive secretion of cystine results in supersaturation and stone formation
  • Cystine precipitates when the cystine concentration exceeds 250ml/L
  • The treatment for cystine stones is alkalinization with potassium citrate (K-citrate) and Thiola, a reducing thiol compound
  • Thiola binds with cysteine to form a mixed disulfide bond (Thiola-cysteine) and is soluble
22
Q

What is the mainstay of kidney stone prevention?

A
  • The mainstay of kidney stone prevention, however, is a high-fluid (3-4 liters/day), low salt diet
  • Patients with recurrent stones should have yearly X-rays, physical exams, and 24-urine collections to monitor for new stone formation