Renal/Urinary Disease Flashcards
(42 cards)
urine phosphorus cyst
got no clinical consequences
Where are the glomeruli
Only found in Cortex
Types of Renal Pathology
- Congenital Malformation (10% of all birth gave this)
- Glomerular disease
- Tubular disease
- Interstitial disease
- Obstructive disease
- Vascular disease
- Neoplastic disease
Kidney Disease places
Intrarenal: Glomerular- Malformation & Interstitial
- Malformation: Tubular
- Interstitial: Vascular
Prerenal: Atherosclerosis, Ischemia
Postrenal: Stones, Tumors
Clinical SIgns of Renal Disease
- Albuminura (Glomerular disease; albumin in urine)
- Cylindruria (Worm live protein aggregat, blocking urinary flow out of the tubular)
- Hematuria (Ominous, blood in urine => prooblem in bladder)
- Pyuria (active infection)
- Protenuria (any of the above excess protein)
- Azotemia-elevated BUN and creatinine (biochemical)
- Uremia-clinically evident azotemia (clinical sign)
- Change (usually decrease) in GFR
Acute Kidney Injury (AKI)
In general tubular necrosis => into lumen => soft and => coagulate urine, cyliduria
- Decreased blood pH (acidosis)
- Systemic edema
- Hypertension
- Increased BUN, creattinine, K+
- Uremia
- Most common cause; Acute Tubular Necrosis (can be a problem in glomerular but not most common)
- Etiology usually ischemia (truma, surgery, childbirth), toxicant and pharmaceuticals
Recovery is good (even tho it kill epithelial lining)
- (if basal lamina remain intact => regeneration)
Acute Kidney Injury GFR
Screenshot
Stage I
Chronic Kidney Disease (GFR)
> 90 mL/min
- Normal
Stage 2
Chronic Kidney Disease (GFR)
60-89 mL/min
-Mild CKG
Stage 3A
Chronic Kidney Disease (GFR)
45-59mL/min
- Moderate CKD
Stage 3B
Chronic Kidney Disease (GFR)
30-44 mL/min
- Moderate CKD
Stage 4
Chronic Kidney Disease (GFR)
15-29 mL/min
- Sever CKD
Stage 5
Chronic Kidney Disease (GFR)
<15 mL/min
- End- stage CKD
Chronic Kidney Disease (GFR)
Irreversible at any stage
Chronic Renal Disease
Consequences
Bilateral=> Involve both kidney
Leaking => smell like urine
- Muscle Wasting (trying to gen N2)
- Uremia (breath out uric acid)
- Dry, yellow skin
- Pruritus (scratch mark all over face and chest-itchy)
- Uremic frost (uric acid form crystals around mouth)
- Nausea
- GI bleeding (too much uric acid in circulation)
- Anemia
- Decalcification of bones (calcium wasting, bone becomes soft -> hyperosita (thick bones but not strong)
- Vitamin D deficiency
- Hypertension
- Edema
- Neuropathy
- Coma, death
Progression variable, Prognosis is poor
-GFR <20-25%
Congenital Malformations
- Agenesis/dysgenesis/alplasia (Kidney is not fully formed)
– Bilateral: fetal death
– Unilateral: Compensation - Horseshoe Kidney: (kidney remain attached)
– Asymptomatic except in pregnant women
Congenital Malformation
Polycystic Kidney
Polycystic Kidney: Genetic
Infantile/Childhood
- Autosomal recessive, mutation of PKD1 (polyastic kidney disease 1)
– Congenital liver fibrosis
Adult:
- Autosomal dominant, mutation of PKD1 for polycystin-1, leading to Ca-induced defects of extracellular matric
– 1:500-1000 individuals
– 75% develop hypertension, 10-30% have brain aneurysms
– Not symptomatic until 4th decade
Kidney Structure
- Glomerulus
- Tubules
– PCTs
– Straight segments
– DCT - Interstitium
- Vessels
- Urine pathways
Glomerulus
- Bowman’s Capsule
- Largely a capillary network (60mmHg)
- Arteriole-Capillary-Arteriole
– Efferent arteriole is smaller than afferent arteriole; help maintain post-capillary BP - Change in size is possible, no change in numbers (if damage, it will not regenerate instead it will compensate)
- Most glmerular disease is IMMUNOLOGICAL
– Immune-complex GN
– Anti-basement membrane GN
Nephritic Syndrome
EXAM QUESTION
- Sudden onset of hematuria (Glomerular cap leaking large material)
- Decreased GFR
- Proteniuria (Glomerular cap leaking large material)
- Azotemia
- Hypertension and moderate edema
- Classically seen in post-streptococcal GN
Underlying mechanism is inflammatory lesion of glomerulus (antibodies, antigen complexes reflected in kidney)
Nephrotic Syndrome
- Hypoalbuminema (plasma albumin <3 gm/dL)
- Hyperlipidemia
- Proteinuria (>3.5gm/24hr)
- Edema/Anasarca-severe 3rd spacing
- Lipiduria
- Most commonly associated in children with Minimal Change Disease
Underlying cause is derangement in glomerular capillaary wall with increased permeability
Immune Complex Glomerulonephritis
Circulating or fixed immune complexes (usually IgG), trapped against glomerular basement membrane
– Associated with long standing Strep infections; in most cases the infectious agen is NOT found in the kidney (circulate in blood, blocked at membrane of glomerulus)
- Activate complement WBCs through cross linking Fc receptors and decoration with Igs
- Deposition of immune complexes gives granular pattern by immunoflurescence (cause unspecific leaks)
Loss of membrane integrity follow in sever cases; most cases; esp. children, follow milder course
- Can result in progressive renal failure, most often in adults (15-50%); may take several decades to appear
Characterized by
– ABRUPT onset of hematuria
– Associated with acute nephritic syndrom
Anti-Basement Membrane Glomerulonephritis
Caused by formation of auto-antibodies against glomerular basement membrane
- Deposition of immune label is linear
- Major cause is confomational change in the alpha-3 chain of Type IV collagen (only need one chain to be defective)
– Similar collagen is found in the lung; consequently kidney and lung lesion may co exist (Goodpasture disease)
Anit-GBM disease is <1% of all GN. However, the disease is very serious and often result in renal failure
Tubules
- PCT
– Convoluted segment (most sensitive to ischemia and toxicants)
– Pars recta (straight segment) - Descending and ascending loop of Henle
- DCT
- Excretory collecting ducts
Infectious agents => Not in kidney