Exam 4 - Chapter 16 Flashcards
(36 cards)
Diagnostic Testing
BUN: Blood Urea Nitrogen
Creatinine levels in blood/urine
GFR: Glomerular filtration rate
Polyuria
Increased amount of urine
Oliguria
Decreased daily output of urine
Anuria
No urine produced
Proteinuria
Increased protein in the urine
Glucosuria
Increased glucose in the urine
Hematuria
Blood in the urine
Pyuria
Pus in the urine
Dysuria
Painful and burning urination
Developmental Disorders of the Kidney
Renal Agenesis (not formed): Bilateral (Potter syndrome: deadly) or unilateral (Unilateral agenesis: leads to hypertrophy of the existing kidney and hyper filtration increases risk of renal failure later in life)
Horseshoe Kidney: fusion of kidneys at the lower pole
Multi-cystic Renal Dysplasia: Usually unilateral. Cysts are
embedded in the connective tissue
Adult Polycystic Kidney Disease (APKD)
Renal parenchyma is replaced with multiple, large cysts. Results in renal failure in adults
Causes: Autosomal dominant. 90% from mutation of APKD1 gene
Symptoms: Hypertension (due to increased renin), hematuria, palpable renal masses, worsening renal failure, Berry aneurysms of the cerebral circulation, hepatic cysts, mitral valve prolapse
Treatment: Can’t prevent renal failure, but HTN treatment with ACE inhibitors may slow progression
Infantile Polycystic Kidney Disease (IPKD)
Closed, small cysts that are not in continuity with the collecting system. Very rare, results in renal failure and death in infants
Causes: Autosomal recessive
Symptoms: CT scan shows multiple cysts
Treatment: None
Nephrotic Syndrome
Massive proteinuria is generally characterized by excretion of more than 4 grams of protein per day
Causes: Membranous Nephropathy (immune molecules form harmful deposits in glomeruli)
Pathology: Unlike disorders with greater disruption of glomerular structure, proteinuria in the nephrotic syndrome is unaccompanied by increased urinary red cells or white cells
Symptoms: Hypoalbuminemia (low alubumin) results from proteinuria and is often marked by a serum concentration of less than 3 g/100 mL, edema results from decreased plasma colloid oncotic pressure
Treatment: Treating underlying causes
Membranous Nephropathy
Immune complexes deposit in glomeruli
Causes: Idiopathic, autoimmune, lupus, infections, drugs
Pathology: IgG deposits in subepithelial locations, spike-and-dome appearance (basically crevices) best seen with silver stain, GBM thickeningType I (subendothelial deposits): Associated with HBV and HCV. Type II (dense deposit disease): Associated with overactivation of complement system
Symptoms: Nephrotic syndrome, edema, proteinuria, azotemia, hematuria, renal vein thrombosis
Treatment: Spontaneous remission, ACE inhibitors
Berger’s Disease (IgA Nephropathy)
Most common nephropathy in the world. IgA deposits in mesangium of glomeruli
Causes: Idiopathic, bacterial/viral infections. NOT autoimmune
Pathology: Mesangial deposits of IgA, increased serum IgA
Symptoms: Hematuria 1-2 days after infection, proteinuria, hypertension, fatigue
Treatment: ACE inihibitors, steroids
Goodpasture Syndrome
Autoimmune disease
Causes: Antiglomerular basement membrane (anti-GBM).
Pathology: IgG antibodies attack alveolar and GBM
Symptoms: Pulmonary hemorrhage and glomerulonephritis
Treatment: Immunosuppressive drugs, corticosteroids
Rapidly Progressive (Crescentic) Glomerulonephritis (RPGN)
Severe and progressive glomerular injury
Causes: Idiopathic, Goodpasture syndrome, Lupus, Berger’s Disease, Wegener granulomatosis
Pathology: Crescent-moon shape between Bowman’s capsule and glomerular tuft
Symptoms: NePHRITic syndrome, hematuria, hypertension, azotemia, and symptoms of the causes
Treatment: Diuretics, ACE inhibitors, immunosuppressive drugs, steroids
Poststreptococcal Glomerulonephritis (Acute Proliferative Glomerulonephritis)
Prototype of nephritic syndrome. Immune complex disease with the antigen of streptococcal origin
Causes: Nephritogenic strains of group A
β-hemolytic streptococci. Unlike rheumatic fever, which chiefly follows streptococcal tonsillitis, it can also occur after skin infections
Pathology: Urinary RBCs, decreased serum C3, azotemia, elevated ASO antibody titer
Symptoms: Hematuria, oliguria, hypertension, nephritic syndrome, and periorbital edema
Treatment: Spontaneous recovery. Complete recovery in almost all children and many adults follows. A very small minority develops rapidly progressive glomerulonephritis
Alport Syndrome
Hereditary nephritis associated with nerve deafness and ocular disorders, such as lens dislocation and cataracts
Causes: Genetic (usually X-linked dominant) results in mutation in the gene for the α5 chain of type IV collagen
Pathology: Thinning and splitting of GBM
Symptoms: Nephritic syndrome, often progressing to end-stage renal disease by 30 years of age, hematuria, erythrocyte cysts, nerve deafness, cataracts, ectopia lentis, corneal dystrophy
Treatment: ACE inhibitors, renal transplant in severe cases
Focal Segmental Glomerulosclerosis
Sclerosis of glomeruli that involves some but not all glomeruli and only a part of those some. Clinically similar to minimal change disease, although it occurs in both children and older patients. More common in African Americans
Causes: Idiopathic, heroin use, morbid obesity, reflux nephropathy, HIV infection, untreated minimal change disease
Pathology: IgM and C3 seen in secrotic lesions, hyalinosis, sclerosis of glomeruli with focal and segmental distribution
Symptoms: Nephrotic syndrome, edema, proteinuria, hematuria
Treatment: Poor prognosis to steroids and resulting in chronic renal failure. Corticosteroids, cyclosporine, ACE inihibitors
Diabetic Nephropathy
Nodular and diffuse thickening of glomerular basement membranes (GBM)
Pathology: Electron microscopy demonstrates a striking increase in thickness of the glomerular basement membrane. Thickening of vascular basement membranes
observable by electron microscopy is one of the earliest morphologic changes in diabetes mellitus.
Symptoms: An increase in mesangial matrix results in two characteristic morphologic patterns: a) Diffuse glomerulosclerosis is marked by a diffusely distributed increase in mesangial matrix, b) Nodular glomerulosclerosis is marked by nodular accumulations of mesangial matrix material (Kimmelstiel-Wilson nodules)
Urinary Stones
Calcium stones (75%): Calcium phosphate or calcium oxalate stones - Increase of Ca concentration
Struvite stones (15%): Staghorn calculi are magnesium phosphate stones that form in alkaline urine, which is commonly found in patients with persistent UTIs
Uric acid stones (5%): Found in gout
Cystine stones (1%): Occur in patients with cystinosis, an inborn error of metabolism
Urolithiasis (Kidney Stones)
Pathology: Increased concentration of salts in urine. Gout will increase the uric acid production due to defective purine metabolism. Increase of Ca ions due to hyperparathyroidism
Urinary tract infection: a) Decrease solubility of salts. b) Bacteria (UTI) are responsible for crystalizing the salts.
Symptoms: High intensity of pain in the back radiating to the right shoulder and groin, hematuria
Treatment: Surgery/wave therapy, drugs which will pass the stone
Urinary Tract Infection (Cystitis)
Bacterial infection in the bladder. Common in young sexually active women and in older men due to BPH
Causes: Most frequently Escherichia coli (normal flora). The most common pathogen in young, sexually active women is Staphylococcus saprophyticus. Klebsiella pneumoniae & Proteus mirabilis (alkaline urine with ammonia scent). BPH (males). Catheter that may carry bacteria. Injury to mucosa by kidney stone which disrupts
protective epithelium allowing bacteria to invade deeper tissue
Pathology: Urinalysis - cloudy urine with > 10 WBCs/high power field (hpf). Dipstick - Positive leukocyte esterase (due to pyuria) and nitrites (bacteria convert nitrates to nitrites). Culture - greater than 100,000 colony forming units (gold standard)
Symptoms: Frequent urination, dysuria, pyuria, hematuria, bacteriuria. No urinary white cell casts
