Exam 4 - Chapter 16 Flashcards
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
Urinary Tract Infection (Pyelonephritis)
Bacterial infection in the kidney. Can be acute or chronic. More frequent in women, especially during pregnancy
Causes: Hematogenous bacterial dissemination to the kidney or by external entry of organisms via urethra into the bladder and then spread upward from the bladder into the ureters (vesicoureteral reflux) and through the ureters to the kidney (ascending infection)
Pathology: Acute - affects renal cortex with sparing of glomeruli. Chronic - assymetric corticomedullary scarring, thyroidization of kidneys
Symptoms: Acute - fever, flank pain, CVA tenderness, WBC casts, leukocytosis, polyuria, dysuria, nauseau, vomiting, diarrhea. Chronic - renal hypertension, ESRD
Treatment: Acute - antibiotics and fluid. Chronic - renal transplant
Acute Renal Failure (Prerenal)
Kidneys can’t filter waste from the blood
Causes: Decreased effective arterial volume (decreased cardiac output, systemic hypovolemia (as in massive burns), or peripheral pooling of blood due to marked vasodilation (as in gram-negative sepsis)), renal vasoconstriction.
Pathology: Renal hypoperfusion leads to decreased GFR, sodium and water retention, concentrated urine, oliguria. Measurement of urinary sodium is diagnostically significant in addition to oliguria. The BUN:creatinine ratio is characteristically greater than 20 due to a combination of both decreased glomerular filtration and increased tubular reabsorption of urea
Symptoms: Oliguria, azotemia, hyperkalemia, urinary Na+ 500, BUN/Cr > 20
Treatment: Fluid/electrolyte management, reversal of underlying cause
Acute Renal Failure (Intrarenal)
Kidneys can’t filter waste from the blood
Causes: Acute tubular necrosis, acute interstitial nephritis, glomerulonephritis, thrombotic microangiopathy
Pathology: Patchy tubular necrosis, tubule obstruction, fluid backflow, decrease in GFR
Symptoms: Oliguria, azotemia, hyperkalemia, urine osmolality
Acute Renal Failure (Postrenal)
Kidneys can’t filter waste in the blood
Causes: Mechanical blockage of urinary flow, BPH, neurogenic bladder, neoplasia
Pathology: Bilateral outflow obstruction, elevated uretal pressure, decreased GFR
Symptoms: Oliguria, azotemia, hyperkalemia, urinary Na+ > 40, BUN/Cr > 20
Treatment: Treatment of obstruction
Acute Tubular Necrosis
Injury and necrosis of tubular epithelial cells which can lead to acute renal failure (intrarenal azotemia)
Causes: Necrotic cells plug tubules; obstruction decreases GFR, renal ischemia (decreased blood supply from prolonged hypotension or shock), crush injury, nephrotoxic drugs (NSAIDs, lead, chemo, post-operative antiobiotics, ethylene glycol
Pathology: Brown, granular casts are seen in the urine, BUN/Cr
Hemodialysis
It substitutes for the functions of the kidneys, which removes waste products from the patient’s blood
Waste products from the patient’s blood diffuse across a semipermeable membrane into a solution (the dialysate) on the other side of the membrane
Two Types:
Extracorporeal (more common): Patient’s circulation connected to artificial kidney machine
Peritoneal (less common): Patient’s own peritoneum used as dialyzing membrane
Renal Transplantation
When kidneys fail, renal transplantation may be attempted
• The kidney is obtained from a close relative or cadaver donor
• The survival of the transplant depends on the similarity of HLA antigens (MHC) between donor and recipient
• Only identical twins will contain identical HLA antigens in their tissues
Hypertensive Nephrosclerosis
Shrunken and scarred kidneys
Causes: Poorly controlled hypertension
Pathology: Mesangial cell proliferation with shrunken glomerular tuft, sclerosis and hyanilization of afferent arterioles
Symptoms: Nephrotic syndrome, proteinuria, hypertension, hypertensive retinopathy, left ventricular hypertrophy
Treatment: ACE inhibitors, dialysis
Wilm’s Tumor
Malignant tumor of infancy and childhood (2 to 4 years of age)
Causes: Deletion of WT-1 and WT-2 genes (cancer suppressor genes), familial or bilateral in 10% of cases
Pathology: Composed of immature cells resembling renal blastoma, presence of mesenchymal elements (bone, cartilage, etc.), large well-circumscribed renal mass, microscopic hematuria
Symptoms: Huge nontender palpable flank mass, fever, abdominal pain
Treatment: Good prognosis when surgery is combined with chemotherapy
Renal Cell Carcinoma
Most common renal malignancy, more common in men, 50-70 years old
Causes: Von Hippel-Lindau disease, deletion on chr 3 and cigarette smoking
Pathology: Secondary polycythemia (results from erythropoietin production), polygonal clear cells (derived from tubular epithelium), invades IVC and spreads hematogenously to lungs, bones, etc.
Symptoms: Classic triad of flank pain, palpable mass, and hematuria. Paraneoplastic syndromes (ectopic EPO, ACTH, prolactin, gonadotropins, and renin) which can cause hypercalcemia
Treatment: Nephrectomy, chemo, radiation
Transitional Cell Carcinoma
Most common tumor of the urinary collecting system and can occur in renalpelvis, ureter, or bladder. It is often multifocal in origin due to the field effect
Causes: Industrial exposure to benzidine or β-naphthylamine, an aniline dye, cigarette smoking
Symptoms: Hematuria, local extension to surrounding tissues
Treatment: Cyclophosphamide, likely to recur after removal
Urinary Bladder Carcinoma
Most common cancer of the urinary tract. Most tumors are transitional carcinomas but may be squamous or adenocarcinomas
Causes: Infections, benign tumors, kidney stones,
Pathology: Diagnosis made on urine cytology and cystoscopic biopsy
Symptoms: Hematuria, dysuria, lower abdominal pain
Treatment: Grade I tumors localized to mucosa—98% 5-year survival but tend to recur. Grade III tumors with metastases—15% 5-year survival
