6. Renal Disease Flashcards
definition of GN
dysmorphic RBCs or RBC casts
protein > 3-3.5 g/day
definition of nephrotic syndrome (4)
protein > 3.5 g/day
hypoalbuminemia < 3.5 g/dL
edema
hyperlipidemia, lipiduria
4 categories of GN based on glomerular involvement
diffuse (all glomeruli)
focal (< 50% of glomeruli)
global (whole glomerular tuft)
segmental (part of glomerular tuft)
acute glomerulonephritis
etiology, onset, mechanism
post-streptococcal (S. pyogenes) infection
1-2 weeks post-strep
antibody complexes against M protein (Spyo) deposit in glomerular membrane
acute glomerulonephritis
s/s, lab findings
fever; edema; periorbital edema; fatigue
hematuria; RBC casts/dysphormics; mild proteinuria
acute glomerulonephritis
treatment, prognosis
supportive
self-limiting
goodpasture’s
etiology, onset, mechanism
viral respiratory infection → cytotoxic antibody attached to glomerular and alveolar basement membranes
goodpasture’s
s/s, lab findings
hemoptysis; dyspnea
hematuria (macroscopic); RBC casts; proteinuria
goodpasture’s
prognosis
leads to chronic GN and end-stage renal failure
Henoch-Schonlein purpura
etiology, onset, mechanism
viral URT infection in children
↓ platelets
renal involvement is an eventual serious complication
Henoch-Schonlein purpura
s/s, lab findings
purpura; blood in sputum and stools
macroscopic hematuria; proteinuria; RBC casts
Henoch-Schonlein purpura
treatment, prognosis
50% make complete recovery
50% → renal failure
Rapidly progressive crescentic glomerulonephritis
etiology, onset, mechanism
associated with SLE
complication of other forms of GN
macrophages damage capillary walls in glomerulus
cells, plasma released into Bowman’s space
crescentic forms: macrophages, fibroblasts, polymerized fibrin
Rapidly progressive crescentic glomerulonephritis
s/s, lab findings
↑ fibrin degradation products, cryoglobulins, IgA deposits
Rapidly progressive crescentic glomerulonephritis
treatment, prognosis
poor prognosis; often terminates in renal failure
most serious acute GN
Membranous glomerulonephritis
etiology, onset, mechanism
associated with autoimmune disorders (SLE, Sjogren’s syndrome, secondary syphilis, hepatitis B, gold and mercury treatments, malignancy)
thickening of glomerular membrane
IgG immune complex deposition
Membranous glomerulonephritis
s/s, lab findings
microscopic hematuria; very high proteinuria
Membranous glomerulonephritis
prognosis
slow progression to nephrotic syndrome (50%)
Wegener’s Granulomatosis
etiology, onset, mechanism
antineutrophilic cytoplasmic antibody (ANCA)
antibody to neutrophils damages small vessels in lungs & glomerulus
Wegener’s Granulomatosis
s/s, lab findings
hemoptysis
macroscopic hematuria; proteinuria; RBC casts; azotemia
immunofixation test (p-ANCA/c-ANCA)
Wegener’s Granulomatosis
treatment, prognosis
possible progression to end-stage renal failure
Membranoproliferative Glomerulonephritis (MPGN)
etiology, onset, mechanism
Type 1—thickening of subendothelial & peripheral capillaries
Type 2—dense deposits in glomerular basement membrane
often in children
Membranoproliferative Glomerulonephritis (MPGN)
s/s, lab findings
variable lab results—hematuria; proteinuria; ↓ serum complement
Membranoproliferative Glomerulonephritis (MPGN)
treatment, prognosis
poor prognosis
Type 1—progress to nephrotic syndrome
Type 2—progress to chronic GN
IgA Nephropathy (Berger’s Disease)
etiology, onset, mechanism
IgA complexes deposited on glomerular membrane
maybe from mucosal infection
children and young adults
#1 cause of primary GN
IgA Nephropathy (Berger’s Disease)
s/s, lab findings
recurrent macroscopic hematuria following exercise
rust-colored urine; proteinuria; glycosuria; casts (cellular, waxy, broad)
IgA Nephropathy (Berger’s Disease)
treatment, prognosis
anti-HTN drugs; low salt, low protein diet
slow progression to chronic GN (50%)
Nephrotic Syndrome
etiology, onset, mechanism
damage to shield of negativity and podocytes; increased permeability
systemic shock ↓ blood flow to kidneys
Nephrotic Syndrome
s/s, lab findings
proteinuria > 3.5g/day; hematuria; hypoalbuminemia (stimulates lipid production in liver); edema
RTEs; OFBs; casts (fatty, waxy, RTE); cholesterol crystals; fat droplets
Nephrotic Syndrome
treatment, prognosis
medication, diet
Minimal Change Disease
etiology, onset, mechanism
1st cause of nephrotic syndrom in children
disruption of podocytes associated with allergic rxn, immunizations, HLA-B12
Minimal Change Disease
s/s, lab findings
heavy edema
other nephrotic syndrome findings
Minimal Change Disease
treatment, prognosis
corticosteroids (may lead to steroid dependence)
Focal Segmental Glomerulonephritis
etiology, onset, mechanism
disruption of podocytes
associated with heroin, analgesics, HIV
partial glomeruli involvement
Focal Segmental Glomerulonephritis
s/s, lab findings
resembles nephrotic syndrome & minimal change disease
hematuria; proteinuria
Alport’s Syndrome
etiology, onset, mechanism
sex-linked or autosomal genetic disorder
collagen IV mutation
lamellated appearance of basement membrane (thinning)
males < 6 yo associated with respiratory infections
Alport’s Syndrome
s/s, lab findings
macroscopic & microscopic hematuria
hearing/vision abnormalities
Alport’s Syndrome
treatment, prognosis
supportive
can progress to renal insufficiency, failure, nephrotic syndrome
Chronic Glomerulonephritis
etiology, onset, mechanism
“slow and silent”
progression of other GN disorders
Chronic Glomerulonephritis
s/s, lab findings
hematuria; proteinuria; glycosuria; casts (cellular, waxy, broad)
↓ GFR; ↑ BUN/creatinine; ↑ phosphate; ↓ calcium
Chronic Glomerulonephritis
treatment, prognosis
dialysis
renal transplant
Diabetic Nephropathy
etiology, onset, mechanism
glycosylated proteins damage glomerular membrane
sclerosis of vascular structure
Diabetic Nephropathy
s/s, lab findings
microalbuminemia (earliest biomarker)
Diabetic Nephropathy
treatment, prognosis
1st cause of end-stage renal disease
strict control of BG, HTN
Acute Tubular Necrosis
etiology, onset, mechanism
ischemic damage to RTEs or presence of toxic substances
shock, trauma, surgery, myoglobin (strenuous exercise), nephrotoxic antibiotics
Acute Tubular Necrosis
s/s, lab findings
oliguria, nocturia, edema, nausea, vomiting, seizures, decreased consciousness, easy bruising, joint pain, flank pain
RTEs, RTE casts; blood strip +; ↓ specific gravity
Acute Tubular Necrosis
treatment, prognosis
correct underlying cause
Fanconi Syndrome
etiology, onset, mechanism
inherited
associated with cystinosis and Hartnum disease or acquired through toxic agents (ex. outdated tetracycline)
general failure of reabsorption in PCT
Fanconi Syndrome
s/s, lab findings
glycosuria; proteinuria; low pH; cystine crystals
Fanconi Syndrome
treatment, prognosis
supportive
Uromodulin Associated Kidney Diseases (UMKD)
etiology, onset, mechanism
autosomal mutation in gene for uromodulin
↑ abnormal uromodulin builds up and damages tubular cells
teenage years
Uromodulin Associated Kidney Diseases (UMKD)
s/s, lab findings
gout (teenage years)
↑ serum uric acid
Uromodulin Associated Kidney Diseases (UMKD)
treatment, prognosis
eventual renal transplant
Diabetes Insipidus
etiology, onset, mechanism
nephrogenic (failure to respond to ADH)—inherited sex-linked recessive or acquired (lithium, amphotericin B, PCKD, sickle cell)
neurogenic (failure to produce ADH)
Diabetes Insipidus
s/s, lab findings
severe dehydration, polyuria
↓ SG; glucose =
nephrogenic—1:1 osmo after ADH injection
neurogenic— 3:1 osmo after ADH injection
Renal Glycosuria
etiology, onset, mechanism
inherited autosomal recessive
failure of glucose active transport
Renal Glycosuria
s/s, lab findings
glycosuria with normal BG
Renal Glycosuria
treatment, prognosis
benign
Renal Tubular Acidosis
etiology, onset, mechanism
distal—defects in distal H+ excretion
proximal—defect that reduces the capacity to reclaim filtered bicarbonate in PCT
voltage-dependent—defects in distal Na+ reabsorption
Renal Tubular Acidosis
s/s, lab findings
metabolic acidosis
Acute Pyelonephritis
etiology, onset, mechanism
ascending infection from lower UTI
rapid onset
Acute Pyelonephritis
s/s, lab findings
urinary frequency, nocturia, burning, lower back pain, malaise, chills
LE +; nitrite +; mild proteinuria; hematuria; WBCs; WBC casts; bacteria; bacterial casts
Acute Pyelonephritis
treatment, prognosis
antibiotics
no permanent damage
Chronic Pyelonephritis
etiology, onset, mechanism
structural abnormalities affecting flow of urine → recurrent infections
Chronic Pyelonephritis
s/s, lab findings
polyuria, nocturia, HTN
LE +; nitrite +; moderate proteinuria; hematuria; WBCs; WBC casts; bacteria +/=; bacterial casts; waxy and broad casts
Chronic Pyelonephritis
treatment, prognosis
permanent scarring of renal tissue
correction of underlying defect
Acute Interstitial Nephritis
etiology, onset, mechanism
allergic reaction to certain medications
onset 1-2 weeks of initial dose
Acute Interstitial Nephritis
s/s, lab findings
skin rash, oliguria, edema
hematuria; proteinuria; urine eosinophils (Hansel stain); no bacteria; WBCs; WBC casts
Acute Interstitial Nephritis
treatment, prognosis
d/c medication
corticosteroids
Cystitis
etiology, onset, mechanism
frequent in women & children
#1: E. coli
Cystitis
s/s, lab findings
urinary frequency, burning
LE +; nitrite +; ↑ pH; WBCs; bacteria
Cystitis
treatment, prognosis
antibiotics
Urethritis
etiology, onset, mechanism
bacterial or viral infection
often STI
Urethritis
s/s, lab findings
dysuria, polyuria, urethral discharge
hematuria; WBCs; bacteria
Urethritis
treatment, prognosis
antibiotics
Acute Renal Failure
etiology, onset, mechanism
sudden loss of renal function
prerenal, renal, or postrenal
Acute Renal Failure
s/s, lab findings
↓ GFR; oliguria, edema, anuria, flank pain, ↓ sensation, ↓ appetite, metallic taste, hiccups, change in mental status, seizure, tremors, nausea, vomiting, bruising, fatigue
urine sediment not distinctive
Acute Renal Failure
treatment, prognosis
often reversible
Chronic Renal Failure
etiology, onset, mechanism
progressive loss of renal function
usually due to DM or HTN
Chronic Renal Failure
s/s, lab findings
GFR
↑↑ BUN and creatinine levels, ↑ K, electrolyte imbalance, ↓ Ca, secondary hyperparathyroidism, ↓ creatinine clearance, metabolic acidosis, anemia
GFR < 25 mL/min; isosthenuria; proteinuria; glycosuria
Chronic Renal Failure
treatment, prognosis
irreversible
control sx
Renal Lithiasis
etiology, onset, mechanism
pH, concentration, urine stasis contribute
increased in the summer, dehydration
increased dietary oxalates and ascorbic acid, cytotoxic drugs, endocrine disorders, foreign body seed, chemical salts in urine ultrafiltrate
Renal Lithiasis
s/s, lab findings
intense pain beginning in flank and radiating forward and downward, vomiting, sweating, frequent urge to urinate
hematuria; ↑ SG; crystals (75% calcium)
Renal Lithiasis
treatment, prognosis
lithotripsy
surgical removal
Polycystic kidney disease
etiology, onset, mechanism
hereditary
fluid-filled cysts form on kidneys
Polycystic kidney disease
s/s, lab findings
HTN, hematuria, back pain, frequent bladder or kidney infections, ↑ BUN & creatinine, anemia
Polycystic kidney disease
treatment, prognosis
4th cause of chronic kidney failure
supportive care
renal transplant
Wilm’s Tumor
etiology, onset, mechanism
develops in fetus
genetic component
Wilm’s Tumor
s/s, lab findings
abdominal pain, swelling of abdomen, hematuria, fever, loss of appetite, n/v, malaise, ↑ BP, constipation, increased growth only on one side of body
Wilm’s Tumor
treatment, prognosis
90% cure rate if localized
bladder cancer prevalence
4th most common cancer in men, 9th in women
pt hx for bladder cancer
older
smoking
most common type of kidney cancer
renal cell carcinoma clear cell type
hemoptysis
Goodpasture’s
Wegener’s granulamatosis
kidney diseases triggered by/associated with infections (5)
acute GN (strep)
Goodpastures (viral resp.)
Henoch-Schonlein purpura (viral URT in children)
IgA nephropathy (maybe mucosal infection)
Alport’s syndrome (males < 6 viral respiratory)
