Test #2 Flashcards
Nephritic characteristics
hematuria
rbc and mixed cell casts
variable proteinuria
Nephrotic characteristics
Marked proteinuria (>3.5 g/day)
Lipiduria
Fatty casts
Nephritic causes
Post-infectious/proliferative glomerulonephritis
IgA neuropathy/vasculitis (HSP)
Lupus nephritis
Thin basement membrane disease
Nephrotic causes
Systemic disease
- Diabetic neuropathy
- Amyloidosis
Minimal change disease
Focal segmental glomerulosclerosis (FSGS)
Membranous neuropathy
Focal Nephritic Patterns
ex: IgA nephropathy
Inflammatory lesions in <1/2 glomeruli
UA: rbc, ~rbc casts, mild protein
Diffuse Nephritic Patterns
ex: post-strep glomerulonephritis (PSGN)
Affects > 1/2 glomeruli
UA: lots of protein, rbc and rbc casts
Edema, HTN, may have renal insufficiency
Nephrotic Patters
Affects many glomeruli
No inflammation/immune complex deposits
Edema, hyperlipidemia, hypoalbuminemia
Ex: Diabetic neuropathy
Poststreptococcal glomerular nephritis (PSGN)
Most common acute nephritic cause
1-3 weeks post strep/3-6 weeks post GABHS
MOA: Glomerular immune complex disease, viral/parasitic infection (rare)
Poststreptococcal glomerular nephritis symptoms and diagnosis
Often asx; discolored urine w/ sediment, edema, HTN
Hx of strep infection w/in 3-6 weeks
UA: gross hematuria, proteinuria
Streptozyme test: antistreptolysin
Biopsy only to r/o other glomerular dx, late presentations w/o clear strep history
Recurrent hematuria episodes indicate:
IgA nephropathy
Not PSGN
Poststreptococcal glomerular nephritis treatment
Supportive
Sodium and water restriction w/ loop diuretic (edema and HTN)
Dialysis w/ acute renal failure
Recovery begins w/in 1st 2 wks
Late renal complications are rare: HTN, proteinuria, renal insufficiency
IgA Neuropathy/Berger’s Disease
Most common primary GN cause
Rare in blacks; 80% 15-35 yo
MOA: Mesangial depositions of IgA complexes
IgA Nephropathy Presentation
1: Gross recurrent hematuria possibly after URI (synpharyngitic)
- flank pain and fever
2: Microscopic hematuria which may progress, mild proteinuria
3: Nephrotic syndrome: protein and lipid urea, fatty casts
- edema, renal insufficiency, HTN, hematuria
IgA Nephropathy diagnosis and treatment
Dx: kidney biopsy -> IgA deposits in mesangium
-Can also indicates cirrhosis, celiac disease, HIV
Tx: BP control (ACEI)
-Severe/progressive: Corticosteroids +/- immunosuppressants
Henoch-Scholein Purpura (HSP)/IgA vasculitis
Systemic vasculitis from IgA complex deposits in tissue
Most common vasculitis in children (3-15 years)
Generally mild in kids, worse in adults
Henoch-Scholein Purpura symptoms
Tetrad:
1: Palpable purpura w/o thrombocytopenia or coagulopathy
2: Arthritis or arthralgia
3: Abdominal pain
4: Renal disease (GN)
Develops over days-weeks, presentation order varies
Spectrum w/ kids to adults: Kids: mild hematuria +/-proteinuria, adults: severe nephrotic syndrome/renal failure
Henoch-Scholein Purpura diagnosis and treatment
Dx: kidney bx - only w/ uncertain dx or severe renal involvement - marked proteinuria/impaired renal function
Tx: Crescentic GN - pulse IV methylprednisone, then oral prednisone
Rare progression to ESRD -> dialysis and transplant
Rapidly progressive glomerulonephritis (RPGN)
Acute GN w/ rapid progression to ESRD
Morphological crescent formation w/in glomerular vessel wall
-fibrin formation w/ macrophage, T cells, cytokines in Bowman’s space
Types of RPGN
1: Anti-glomerular basement membrane (GBM/Goodpasture syndrome)
- anti-GBM abs in lungs and glomerulus
2: Immune complex RPGN - deposit in glomeruli
- IgA Nephropathy, PSGN, lupus nephritis
3: Pauci-immune RPGN - necrotizing GN and vasculitis
- ANCA positive, systemic vasculitis symptoms
RPGN symptoms
Insidious - fatigue and edema
Acute - macroscopic hematuria, oliguria, edema, renal insufficiency
GBM - pulmonary hemorrhage, hemoptysis, pulmonary infiltrates, dyspnea
RPGN Diagnosis and Treatment
UA: hematuria, rbc casts, proteinuria
Increase BUN/Creat, renal bx to confirm
Serologic assay for type
Tx: Pulse methylprednisolone, PO cyclophosphamide, consider plasmapheresis
-treatment gets more specific w/ bx results
Catch early to minimize irreversible injury
Dark granular and epithelial casts in urine indicate:
Pure acute tubular necrosis
Crystal particles in urine
Crystalluric acute renal failure
wbc and wbc casts in urine:
Acute interstitial nephritis
rbc and rbc casts in urine:
Proliferative/necrotizing glomerulonephritis
Prerenal UNa, BUN/Creat, FENa
Urine Na: <20
BUN/Creat: >20:1 (>20)
FENa: <1
Intrinsic UNa, BUN/Creat, FENa
Urine Na: >20
BUN/Creat: <10:1 (<20)
FENa: >2
Postrenal UNa, BUN/Creat, FENa
Urine Na: variable
BUN/Creat: 10-20:1 (<20)
FENa: variable
Acute Interstitial Nephritis
Renal lesion causes creatinine clearance decline
Drugs most common cause - PCN, cephalosporin, sulfa, NSAIDs, Rifampin, Dilantin, Allopurinol
Infections dx also cause: strep, leptospirosis, CMV, Histoplasmosis, Rocky Mountain Spotted Fever
Immunologic causes: Lupus, Sjogren’s Sarcoidosis, Cryoglobulinemia
Acute Interstitial Nephritis sx and tx
Sx: fever, hematuria, peripheral eosinophilia, rash
-UA: rbc, +/- wbc/wbc casts, proteinuria (NSAIDS)
Tx: Supportive, remove cause
- 1-2 week high dose steroids if persistent
- rare progression to ESRD
Proteinuria monitoring
Initial assessment w/ new HTN, DM, hematuria, decreased GFR
Annual monitoring: Bx proven GN, reflux neuropathy, DM
Routinely monitor pts on nephrotoxic agents
Common CKD microorganisms
Staphylococcus
E. coli
Klebsiella (hospitalized pts w/ pulmonary infections)
Endocarditis prophylaxis
2g Amoxicillin OR 600 mg Clindamycin 1 hour before dentist
Immunizations and Dialysis
Screen for Hep B and C before you start on dialysis/put on transplant list
Influenza and Pneumococcus vaccine (revaccinate every 5 years)
CKD Medications to avoid
NSAIDs
Metformin if SCr >1.5 (men) 1.4 (women)
Magnesium-containing meds (laxatives, antacids)
Caution w/ Abx (PCN, cephalosporin, sulfa, fluroquinolones)
Renal Cell Carcinoma
1 renal cancer - men (60-80yo)
Originates in renal cortex
Rick: smoking, HTN, obesity, acquired kidney cystic dx
Clear Cell Carcinoma
PCT - most common RCC, Chromosome 3P deletion
Solid/less cystic, typically invades vasculature
Microscopic: lipid and glycogen cytoplasm, bland cells w/ poor differentiation
-forms solid nest, tubules w/ fine vasculature
Papillary Carcinoma (Chromophil)
PCT, trisomy 7, 16,17
Better prognosis than clear cell
Microscopic: delicate vascular cores w/ overlying tumor cell layer
-Psammoma bodies = necrosis/calcification @ tips
Chromophobe RCC
Cellular sheets darker than clear cell
Arise in CD intercalated cells, lower progression risk than clear cell
Microscopic: pink (eosinophilic) cell sheet w/ perinuclear halos
Collecting duct carcinoma (Bellini duct carcinoma)
Aggressive, affects young and Black
Rare
Oncocytoma
Oncocytes - C-met oncogene mutation
Well-differentiated, very eosinophilic granular cytoplasm
CD intercalated cells
Usually unilateral and single, mets are rare
RCC Clinical features
Triad: Flank pain, gross hematuria, palpable renal mass
Nonspecific features: fever, fatigue, weight loss, scrotal varicocele, paraneoplastic syndrome
Usually present late, asx early
Dx: US then CT
Refer cysts to urologist
RCC common metastasis sites
Lung
Abdominal lymph nodes
Bone
CT w/ a suspicious X-ray, bone scan/PET scan to locate
RCC Treatment
Surgical removal - radical nephrectomy or
-Partial if <4 cm, unilateral tumor
Radical = take everything to Gerota’s fascia and adrenal, +/- part of IVC
RCC Staging
Stage 1: <7cm, limited to kidney - 95% 5 year survival
Stage 2: >7cm, limited to kidney - 88%
Stage 3: tumor in major vein/adrenal/Gerota’s fascia/regional lymph node - 59%
Stage 4: Tumor beyond Gerota’s fascia or in >1 regional lymph node - 20%
Wilm’s Tumor (Nephroblastoma)
Most common renal tumor in kids
Abnormal renal development - metanephric blastoma proliferation w/o tubular or glomerular differentiation
Risk: aniridia (iris), hemihypertrophy, undescended testes, hypospadias (ureter)
Wilm’s Tumor symptoms and diagnosis
Sx: palpable mass, abdominal pain, HTN, hematuria, rarely bilateral
Dx: US and contrast CT, excision/bx for definitive diagnosis
Wilms Tumor staging
Stage 1: unilateral, completely removable
Stage 2: cancer is beyond the kidney, but still completely removable
Stage 3: cancer is contained to abdomen, cannot remove completely
Stage 4: mets to lungs/liver/bone/brain
Stage 5: cancer in both kidneys (bilateral tumors are rare)
Wilms Tumor treatment and appearance
Chemo for all
Radical nephrectomy for stages 1-4, get as much out as possible
Stage 5 - radical nephrectomy, pt must be on transplant list
Large, single, well-circumscribed tumor
-less hemorrhage than RCC, can have cyst formation
Benign renal tumors
Renal papillary adenoma - Cortical tubules, trisomy 7 and 17
Renal fibroma/Hamartoma - small, benign fibrous nodule in renal pyramids
Angiomyolipoma - blood vessels, muscle, and fat => occur w/ tuberou sclerosis, easy to spot on radiograph
Can’t distinguish benign from malignant until excised and biopsied
Transitional Cell Carcinoma (TCC)
Transitional epithelium in urinary tract - calyces to uretal orifice
Smoking, male, 60-70 yo, black
Sx: hematuria, renal colic, hydronephrosis
w/u: urine cytology, cystoscopy, IVP
Tx: radical nephroureterectomy and chemo
Renal Sarcoma
Rare, mesenchymal cell tumor
Grow fast and big, peak incidence ~5th decade
Sx: abdominal pain, palpable mass, gross hematuria
Dx: CT
Tx: surgical excision
Renal abscess
Hematogenous or UTI origin with obstruction
Enterococcus (E. coli) or staph
Sx: fever, chill.s abdominal pain, weight loss, hematuria
-looks like acute pyelonephritis
Dangerous w/ DM or advanced
Renal abscess diagnosis and treatment
Ua: wbc, bacteria, protein hematuria, pyuria
CT for dx after UA, CBC (leukocytes), ESR/CRP = inflammation
Tx: Ampicillin + aminoglycosides + I&D if >5cm
Nephrectomy is last resort
Acute pyelonephritis
Affects renal cortex, spares glomeruli and vessels
UA: wbc casts - formed in DCT
E. coli, proteus, Klebsiella, enterobacter
Treat aggressively in DM, pregnancy to prevent abscess
Emphysematous Pyelonephritis
Necrotizing infection w/ gas formation
In poorly controlled DM, immunocompromised
Rapidly progressive -> fulminant sepsis w/ high mortality
Acute Pyelonephritis symptoms and diagnosis
Sx: Shaking chills, fever, arthralgia/myalgia, flank/CVA pain
-urgency/frequency urination, V/D in peds
Dx: UA: wbc casts, bacteria, hematuria - culture
Get blood cultures and CBC (left shift)
CT for dx - hydronephrosis or inflammation/infection
US for obstruction
Acute Pyelonephritis Treatment
Ampicillan (IV) - until 24 hours after fever resolves
Cipro/ofloxacin/Aminoglycosides/Bactrim PO 14 days after
Follow up w/ urine culture to confirm resolved
Refer if complicating factor (stone, reflux, tumor, neurogenic bladder)
Watch for sepsis: tachypnea, AMS
Chronic Pyelonephritis hallmarks
Recurrent/persistent renal infections, usually w/ major anatomical abnormalities (VUR)
Asymmetric corticomedullary scarring/thyroidization
Eosinophilic casts in tubule
Chronic Pye and TEA: thyroidization, eosinophilic casts, asymmetric scarring
Vesicoureteral reflux (VUR)
Kids w/ UTI - screen
Hydronephrosis @ birth, frequent UTIs, bedwetting
Primary: congenital muscular deficiency
Secondary: bladder outlet/functional obstruction
Detect w/ UA, VCUG and US - febrile/male UTI, <5yo w/ UTI
Chronic Pyelonephritis symptoms and diagnosis
Sx: fever, lethargy, N/V, flank pain, dysuria, failure to thrive (kids)
Dx: UA: wbc, bacteria, hematuria
IVP is test of choice - calyceal dilation and blunting w/ cortical scars
VCUG, cystoscopy to document VUR
Chronic Pyelonephritis Treatment
Stage 1&2: Chronic Abx prophylaxis until puberty - Amox, Bactrim, Septra, Nitrofurantoin
Stage 3&4: VUR = surgery w/ ureter reimplantation
-Surgery indicated w/ noncompliance, reflux past puberty, breakthrough infections
Aggressively tx UTIs
Dietary and BP control, routinely screen pregnant and FH
Xanthogranulomatous pyelonephritis (XPN)
Chronic obstruction complication w/ infected stones
Massive kidney destruction, need immediate nephrectomy
Sx: adults - looks like pyelo w/ palpable flank mass and CVA tenderness
Children: type 1 affects genders equally, hits entire kidney
Type 2 hits girls, looks like Wilm’s tumor
1/2 have palpable mass, growth/weight retardation
XPN diagnosis and treatment
Dx: UA: pyuria, bacteriuria, culture reveals G(-) organism
-E. coli, Proteus, Klebsiella; staph is rare
Anemia, increased ESR, LFTs w/ hepatomegaly
Tx: surgical removal + Abx
-can be partial if localized (kids) or bilateral dx
Cystitis
Coliform (E.coli)/G+ (entercoccus) bladder infection
-Viral may occur in kids
Sx: irritative voiding, suprapubic pain, hematuria
Dx: UA - leukocyte esterase, nitrites, +/- blood
Tx: 1-3 days Nitrofurantion (pregnancy), Bactrim/Septra, fluroquinolones
Additional testing if male, recurrent, anatomic abnormality
Nephrotic Syndrome Pathophysiology
Glomerular capillary wall breakdown/Electrostatic charge lost
Proteinuria occurs = Vit D deficiency, PTH increase (low Ca)
-24 hour UA to quantify protein loss
Hypoalbuminemia = decreased oncotic pressure = edema and hyperlipidemia
Hyperlipidemia from increased hepatic synthesis = lipiduria
Minimal Change Disease
Nephrotic Syndrome in kids
Children, Adults w/ NSAIDs
Mild mesangial cell proliferation, flattened podocytes
Idiopathic, drugs, allergies, HL/Leukemia
Tx: Steroids 4-8 wks, 16 for adults
-continue after proteinuria resolves
Focal Segmental Glomerulosclerosis (FSGS)
Nephrotic syndrome
Mesangial collapse and sclerosis in 1/2 glomeruli
Black, idiopathic nephrotic syndrome
Secondary cause: HIV, obesity, DM, lupus, nephrotoxic meds/chemicals
Tx: primary: diuretics, ACEI, statins, high-dose steroids 4-16 wks
Membranous Nephropathy
Most common nephrotic syndrome in adults (5th-6th decade)
Basement membrane thickened w/ immune complex or electron dense deposits
Primary: idiopathic, autoantibodies
Secondary: Hep B/C antigenemia, AI, CA, drugs (gold, captopril, NSAIDs)
Protein leaked despite thickening due to damage electrostatic charge
Nephrotic Syndrome Complications
Infection
Edema
Hypovolemia
HTN
Acute renal failure
Protein malnutrition
Thromboembolism (hypercoagulable w/ hypovolemia)
Vitamin D/Calcium deficiency
Nephrotic Syndrome diagnosis and treatment
24 hour UA
Kidney biopsy - definitive Dx
Triad: proteinuria, edema, hypoalbuminemia
Tx: ACEI/ARB for proteinuria
- diuretics/sodium restriction (edema)
- Statins until cured (hyperlipidemia)
- Anticoagulate w/ DVT (hypercoagulability)
Systemic disorders causing Nephrotic disease
Amyloidosis
Diabetic Nephropathy
HIV-associated nephropathy
Hepatitis C
Multiple Myeloma
Sickle-cell disease
Tuberculosis
Gout
Amyloidosis
Protein deposits in organs (mesangium and capillary loops)
Dx: UA w/ amyloiduria, biopsy, CT to evaluate extent
Tx: Dialysis, progress to ESRD w/ in 2-3 years
5 year survival (w/ heart affected too) <20%
Diabetic Nephropathy
Most common ESRD cause - not always diabetes-induced
-Check onset, rbc/casts, another systematic dx, or ACEI/ARB
Microalbuminuria = screen w/ dipstick, 24 hour test to confirm
Intraglomerular HTN and hyperglycemia contribute to destruction
Tx: control sugars, BP, lipids, weight loss, Na restriction, loop diuretic
HIV-Associated Nephropathy
Nephrotic presentation
Need renal biopsy to confirm = FSGS pattern
HAART slows progression, consider steroids + cyclosporine and ACEI
Systemic Lupus (SLE)
Nephritic presentation most common
Monitor UA and chem panel
Biopsy to confirm
Tx: steroids
Different types - membranous nephropathy is worst
Hepatitis C
Mixed nephrotic/nephritic pattern
80% ESRD pts also have this
Hematuria, proteinuria, HTN, anemia, hypocomplementemia
Tx: only w/ poor renal function, nephrotic, increased HTN, or fibrosis on bx
-INF to suppress viremia and improve renal function (9month dose)
SE INF: flu-like, weight loss, fatigue, fever
Multiple Myeloma
Malignant plasma cells w/ Bence-Jones protein loss
Dx: serum electrophoresis w/ Bence-Jones on UA + hypercalcemia and urea
Tx: Correct Calcium, volume
- Chemo for underlying Ca
- plasmapheresis doesn’t help kidney
Sickle-cell disease
Nephrotic presentation
Papillary necrosis
Hematuria, isosthenuria (urine osmolality = serum), proteinuria
Tx: Hydration, control dx
Tuberculosis
Microscopic pyuria w/ sterile urine - culture for Dx
-need high suspicion/positive PPD for media
Tx: treat TB
Gout
Overproducers or Underexcretors of uric acid
PCT dysfunction results in uric buildup
Tx: diet, hydrate, Allopurinol/Colchicine (reduce uric acid)
Acute Renal Failure/Acute Kidney Injury
Abrupt (w/in <48 hrs) decline in kidney function
-Increased SCr or decreased output or dialysis needed
Sx: N/V, malaise, HTN, pericardial effusion/rub, arrhythmias, abdominal pain, encephalopathic changes
BUN and Creatinine increases
BUN: burn, tetracycline, steroids, fever, GI bleed, catabolic state
-converted from ammonia in liver
Creatinine: secretion blocked by cimetidine or Trimethoprim
Acute Kidney Injury labs
Increased BUN/Creat, hyperkalemia, hyperphosphatemia
Decreased GFR, hypocalcemia, anemia
Platelet dysfunction
Anion gap metabolic acidosis
Pre-renal AKI
Lack of blood flow to glomerulus
-ACEI/ARB (efferent) or NSAIDs (afferent) cause vasodilation
Urine has low sodium, high osmolality due to low perfusion-> increased Na/H2O absorption
Tx: underlying cause, maintain euvolemia and electrolytes
-Avoid nephrotoxic drugs, may need short dialysis course
Post-renal AKI
Reversible, least common AKI cause (BPH usually)
Sx: olig/anuria, lower back/abdominal/flank pain, enlarged prostate/pelvic mass (rectal exam), distended bladder
Dx: US, Catheterization, CT for stones/hydronephrosis
-BUN/Creat 10-20:1
Tx: Bladder catheter, refer to Urology for stent/resection/nephrostomy
Intrinsic AKI
Most common AKI
Caused by:
- Acute Glomerulonephritis
- Acute Interstitial Nephritis
- Acute Tubular Necrosis
- Contrast Nephropathy (ATN form)
Acute Glomerulonephritis
Inflammation/proliferation of glomerular tissue
-damages basement membrane, mesangium, capillary endothelium
Sx: rbc casts, significant proteinuria
PSGN, Systemic (lupus, Wegeners, Goodpasures)
Acute Interstitial Nephritis
Medications, bacteria/viral/fungal infection
Eosinophils on UA
Maculopapular rash, fever, arthralgias
Acute Tubular Necrosis
Most common intrinsic injury
Ischemia, sepsis, nephrotoxic drugs -> tubules fail to function
UA: Deeply pigmented, coarse granular casts are hallmark
Nephrotoxic drugs
Aminoglycosides
Ampho B
Chemo
Acyclovir
Ethylene glycol
Sulfa
Cephalosporins
Contrast Nephropathy
Form of ATN
24-48 hours post exposure
Prevention: minimize contrast, Mucomyst, hydrate, stop Metform for 48 hrs after
Fractional excretion of sodium and urine sodium concentration (FENa)
Determine if AKI cause is prerenal or ATN
100* (UNa x SCr)/(SNa x UCr)
AKI Management and general workup
Maintain euvolemia, electrolytes, BP
- stop potentially nephrotixic meds
- may need temporary dialysis
Workup: Assess volume status, UA, CBC, BUN/Creat (BMP), FENa
Respiratory acidosis
Increase ventilation to correct
Low pH with high CO2
Causes: CNS depression, hypoventilation, impaired respiratory muscle function, pulmonary disorders
Respiratory Alkalosis
Increased pH with decreased CO2 - hyperventilation
Causes: Psychological response, medications, increased metabolic demand, CNS lesion
Metabolic Acidosis
Lack of bicarb OR too much acid
- GI/renal loss
- Renal failure, DKA, ASA overdose, hypoxic tissue
Anion gap narrows down etiology
Increased Anion Gap Metabolic Acidosis
MUDPILES
Methanol intoxication
Uremia
DKA/Alcoholic
Paraldehyde
Isoniazid/Iron overdose
Lactic acid
Ethylene glycol
Salicylate overdose
Anion Gap
Na - (HCO3+Cl)
Normal = 12 +/-4
>20 = High serum AG => metabolic problem always
Non-Anion Gap Metabolic Acidosis
USED CAR
Ureteral-sigmoid diversion (pee into intestine)
Small bowel fistula/Saline administration
Endocrinopathies (Addisons, HyperPTH)
Diarrhea
Carbonic anhydrase inhibitors
(hyper)Alimentation (supplementary/artificial nutrition)
Renal tubular acidosis
Metabolic Alkalosis
Too much bicarb
Gastric suctioning, vomiting, diuretics, antacids
Check Cl here -> chloride-responsive if UCl <10
-Chloride-resistant if UCl> 10 => Mineralocorticoid problem
Contraction alkalosis with large volume loss (diuretics) but bicarb remains the same
High serum anion gap
R/o DKA/alcoholic or lactic acidosis
Delta Gap
Used for Metabolic acidosis
Calculate how abnormal AG is
measuredAG - 12 = change anion gap
24-HCO3 = changed bicarb
AG>BC = metabolic acidosis also present (mixed disorder)
AG<bc></bc>
<p>AG = BC +/-2 = no additional issue</p>
</bc>
Winter’s Formula
Metabolic acidosis
Determine if underlying concomitant respiratory disorder
PaCO2 = 1.5(HCO3)+8 +/-2
OR PCO2 = digits of pH
PCO2>PaCO2 = concomitant respiratory acidosis
PCO2<paco2></paco2>
<p>+/-2 = each other => no underlying disorder</p>
</paco2>
Summer’s formula
Metabolic Alkalosis
Calculate respiratory compensation
PaCO2 = 0.7(HCO3 +21) +/-2
PCO2>PaCO2 = respiratory acidosis
PCO2
