Kidney Exam Flashcards
Anuria
Urine output less than 100 ml/day
Hypotonic fluid
Less than 270
Hypertonic fluid
Greater than 300
Potter sequence
Physical appearance resulting from oligohydramnios-
Beak like nose, small receding chin, low set ears, abnormally bent lower extremities.
Pulmonary hypoplasia- most life threatening component of potter sequence
Bilateral agenesis
Most are still born and have potter sequence, often associated with other congenital anomalies
Unilateral agenesis
Contra lateral kidney undergoes hypertrophy, may lead to progressive glomerular sclerosis from the overworked kidney
Renal hypoplasia
Reduction in renal mass, 6 or fewer renal lobes, no histological malformations
Renal dysplasia
Undifferentiated tubular structures surrounded by primitive mesenchyme, cysts often form around abnormal tubules, undifferentiated tubules and ducts lined by cuboidal or columnar epithelium, cartilage
Renal dysplasia clinical signs
Palpable flank mass, potter sequence, pulmonary hypoplasia
Autosomal dominant polycystic kidney disease
Numerous cysts within the renal parenchyma
- PKD1 and PKD3 gene mutations, polycystins
- inflammatory mediators, destruction
Enlarged kidneys bilaterally, contours distorted with numerous cysts, filled with fluid, liver cysts and berry aneurysms
Autosomal recessive polycystic kidney disease
- PKKHD1 mutation, chromosome 6, fibrocystin and polyductin
- cystic transformation of collecting ducts with smooth outward appearance
Usually die in perinatal period from pulmonary hypoplasia by oligohydramnios and large kidney size, hepatic fibrosis leading to splenomegaly and portal hypertension
Glomerulocystic disease
Dilation of bowman’s capsule in many glomeruli, mutation in hepatocyte nuclear factor-1 beta
Small round cysts, dilation of bowman’s capsule
Medullary sponge kidney
Multiple small cysts in one or more of the renal papilla a, lined y cuboidal or columnar epithelium and arise from the collecting ducts in the renal papillae, usually bilateral
Usually asymptomatic, 30-60 flank pain, dysuria, hematuria, gravel in urine
Acute kidney injury
Sudden decline in GFR over days to weeks, GFR less than 10 ml/min, CR increases by 1-1.5 mg/dL daily
Prerenal acute failure
Transient renal hypoperfusion from hypotension, decreased cardiac output, decreased arterial blood volume
Postrenal acute renal failure
Obstruction of the urinary tract
Intrinsic acute renal failure
Acute glomerulonephritis, acute interstitial nephritis, acute tubular necrosis
Prerenal azotemia
Most common cause of acute kidney injury, renal hypoperfusion
Prerenal acute kidney injury
BUN:Cr ratio >20:1, increased urea reabsorption
Hyaline casts, >1% sodium excretion, kidney reabsorbs salt and water avidly
Post renal azotemia
Least common of acute kidney injury, urinary flow from both or one kidney is obstructed
Post renal AKI
Urethral obstruction (anticholinergics), bladder calculator neoplasms, pelvic or retroperitoneal neoplasms, bilateral ureteral obstruction, retroperitoneal fibrosis
Intrinsic renal failure
Tubular, glomerular, vascular, interstitial
Oliguria
Urine output less than 500 ml/day
Acute tubular necrosis
Tubular damage, initiation phase, maintenance phase, recovery phase
85% of intrinsic acute kidney injury
Acute tubular necrosis initiation
Ischemia, a continuum of pre renal azotemia
Acute tubular necrosis maintenance
Stabilization of GFR at a very low level, usually lasts 1-2 weeks, complications occur
Acute tubular necrosis recover
Regeneration of tubular epithelial cells, abnormal diuresis sometimes occurs causing salt and water loss and volume depletion
Acute tubular necrosis labs
Hyperkalemia (lysis of muscle cells or impaired excretion)
Hyperphosphatemia (cannot be excreted)
Brown urine
BUN:Cr is
Acute interstitial nephritis
Interstitial inflammatory response with edema, cell mediated response, 70% drug hypersensitivity, 15% infection
Drugs: NOT dose dependent
Acute interstitial nephritis findings
Fever, rash, arthralgias, serum eosinophilia, WBC CASTS ARE PATHOGNOMONIC, urine eosinophils
Nephritic syndrome
Involvement of cell proliferation,
Hematuria, proteinuria, hypertension, reduced GFR
Volume overload, hyperkalemia, metabolic acidosis, edema, congestive heart failure
Decreased C3
Alternative pathway activated
Decreased C4
Classical pathway activated
Kidney biopsy
Glomerular cellularity, thickness of GBM, histopathology, determines presence or absence of crescents
Light microscopy
Nature of glomerular disease using stained sections of the kidney biopsy
Immunoflorescence
Determines nature of the causative immune process
Electron microscopy
Location of election dense immune deposits and degree of injury, integrity and thickness of GBM, forms of podocytes injury
Rapidly progressing glomerulonephritis lab findings
> 50% of glomeruli on biopsy will have crescents, trapped immune complexes
Immunofluorescene: IgG, IgA, C3 granular pattern
Electron microscopy deposits in sub epithelium, subendothelial, mesangium
RPGN goodpasture’s syndrome
Anti-GBM antibodies, hemoptysis
Immunoflorescence:IgG, C3 linear pattern
Electron microscopy: widening of GBM
RPGN wegener’s granulomatosis, polyarthritis
No immunoglobulin or deposits
Post streptococcal glomerulonephritis
Pathology
Signs/symptoms
Groups A beta hemolytic streptococci, trapped immune complexes
Edema, oliguric, cola colored uringe, hypertension, ASO levels high, C3 low
PSGN biopsy
Microscopy: diffuse proliferation GN
Immunoflorescence:IgG and C3 in granular pattern in mesangium along capillary basement membrane
Electron Microscopy: large, dense sub epithelial deposits or humps