Renal/Urinary Disease Flashcards
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
Tubule Diseases
- Ischemia (post-surgical, truma)
- Nephrotoxic (mercury, lead, antifreeze)
- Drug-induced (antibiotics, diuretics)
- Other primary renal disease (eg, nephritis, hypertension)
Acute Tubular Necrosis
Clot in lument
- No passage of urine
Ethylene Glycol Tubule Necrosis
Antifreeze disrroys tubules
- Oxylate crystals
– Need to transplant kidney
Tubulo-Interstitial (Connective tissue in between) Disease
- Interstitial nephritis-nonbacterial
- Pyelonephritis (acute/chronic)-bacteria
- Drug-induced nephritis
– Analgesic nephropathy-generally multiple drugs: phenacetin, aspirin, acetaminophen
— Immune case likely Type I hypersensitivity, more rarely Type IV
– Antibiotic nephropathy: sulfonamides, synthetic penicillins, rifampin, NSAIDs, AmphoB
Pyelonephritis
Caused by infection, ascending infections; most commonly E.coli or other gram negative bacteria or hematogenous infection (less common) (Fever, flank pain, pyuria)
- Can be acute or chronic (chronic can lead to chronic renal failure)
- Antibiotics successful but reinfection is common
- More common in females (10:1); incidence in males increase with onset of prostate disease
Associated with:
- UTIs
- Sexual activity
- Obstruction (stones, BPH, tumors)
- Diabetes
- Vesicoureteral reflux (VUR)-ascending infections
- UT mainpulation (catheterization). Candida common organism
- Pregnancy
- Immunosuppression/immunodeficiency
Vessels
Ischemia(most commonly thrombo) emboli, often from recent MI with mural thrombi, or hypovolemia
Hypertension, particularly when coupled with diabetes
- Essential hypertension is very common, will cause wide-spread renal injury and symmetrical atrophy
- Malignant hypertension-much less common
– Extremely serious. BP>200/120 mm
– Requires prompt, aggressive medical intervention
– Will cause renal vascular injury; may cause stroke
– Even with treatment, 5-year survival 50%
Arteriolonephrosclerosis: caused by hypertension
Hyaline degeneration of artery/arteriole walls
Virtually all kidney disease will secondarily affect renal vessels
Renal Hypertension
Benign Hypertension
- Major target: Small arterioles
- Cause vessel narrowing and medial thickening
- Resulting ischemia (from narrowing) leads to interstitial fibrosis, tubular atrophy, glomerulosclerosis
- Cortical surface is finely granular, capsule is adherent
- Cause some degree of functional effect, such as decreased GFR
Rarely a direct cause of death except in African Americans via uremia and renal failure
Malignant Hypertension
Retina of patient
- Hemmorage of retina vesse
Not much was there
Urine Pathway Obstruction
Infection
Stones
Carcinoma
Prostatic hperplasia (males)
Kidney Stones (Urolithiasis)
Common: 5-10% of individuals during lifetime; M>F
- 80% are calcium stones
- Magnesium ammonium phosphate stones (10%)
– Associated with urea splitting organism such as Proteus ssp.
– Both associated with persistently alkaline urine
- Uric acid and cysteine stones (6-9%) seen with acidic urine
Generally unilateral (80%), but may be multiple in that kidney
- Tendency to form stones are familial
- Occur in setting of urine stasis, infection, metabolic disease, change in urinary pH, urothelial trauma; whenever conditions of super-saturation exist
- Often present with flant pain radiating to groin and gross hematuria (termed renal colic)
May pass spontaneously if small; surgery or lithotrips may be required if large and cause obstruction
- Long term obstruction may lead to hydronephrosis and predisposes to recurrent bacterial infection
What type of stone is associated with acidic urine
Uric acid and cysteine stones (6-9%)
Renal Cell Carcinoma
Most arise from tubular epithelium
- Most common in males (2X) in 6th-7th decade; 2-3% of all cancers; Overall mortality is 40%
- Tobacco strongest risk factor. Genetic factors associated (loss or inactivation of von Hippel-Lindau gene VHL) on chromosome 3p
- Incidence greatly increased (>30x) with chronic dialysis and associated polystic disease
- Present with painless hematuria, flank pain and palpable mass
- Cancer present in multiple histological forms with distinctly different prognoses
- May give many forms of paraneoplastic signs-polycythemia, hypercalcemia, change in secondary sexual characteristics, hypertension, fever of unknow orign
- Frequenly have metastasized to lung and/or bones when found
- Metastases may resolve (rarely-not cured) with removel or primary tumor (doesn’t response to chemo or radio therapy)
Wilms Tumor (Nephropblastoma)
Treatable by chemo and radiation
- young children under 4
Blastoma in name mean embronic
Disease of Urinary Bladder
Cystitis and UTIs are primarily a disease of adults
- Most common cause of cystitis is bacterial infection: E. coli, Proteus, Klebsiella, Enterobacter. Also fungi, and Schistosoma in the middle east
- Associated with diabetes, obstruction, theraputic radiation, catheterization
- Bladder infection is more common in women
- May give rise to ascending pyelonephritis
- Symptoms: frequency (every 15-20 min), lower abdominal pain, and dysuria
Bladder Cancer
Urothelial Cancer is preferred but Transitional cell is frequent
Present as painless hematuria with M:F ratio of 3:1 (50-80 age)
- B-naphthylamine increase risk 50x
- Smoking is the most common risk factor
- Tumor penetrates bladder wall and has a high recurence rate (5-year survival 60%)
Cause of death is urinary obstruction rather than metastasis
Urothelial Cancer
Ureters and renal pelvis
Rarer than bladder but have poorer prognosis with <10% and 50% 5-year survival
In areter => prognosis terrible <10% survival
Prostate Gland
Exocrine gland which surrounds the proximal urethra
- Hyperplasia occurs in the periurethral transition zone
- Cancer arises in the periphery of the gland
- Hormone responsive
- Supplies 20-30% of seminal vol; semen is slightly alkaline to neutralize pH in vagina; this prolongs it’s life
- Prostate secretes PSA
- Normal: 11 grams
Skene glands of female are classified as female prostate glands; skene glands produce PSA
Benign Prostatic Hyperplasia
BPH
Frequency increase with age; by 80 years, 90% of males will have BPH
- Result from action of both androgens and estrogen
- DHT (produced by action of 5a-reductase) is a major mediator of prostate
- Weak urinary stream, hesitancy, urgency frequency, incomplete bladder emptying, nocturia, incontinence, UTI
- May cause urinary obstruction
- Does not progress to cancer
