Nephrology & Urology Flashcards
Characterize nephrotic syndrome
- proteinuria
- hypoalbuminemia
- hyperlipidemia
- edema*
what is nephrotic syndrome (anatomy)
damage to the glomerular causes PROTEIN loss in urine –> hyPOalbuminemia –> *EDEMA
name 3 primary idiopathic causes of nephrotic syndrome
1) minimal change disease
2) focal segmental glomerulosclerosis (FSGS)
3) membranous nephropathy
80% of children that have nephrotic syndrome present with this type
minimal change disease
Tx of choice for minimal change disease
Prednisone
what is seen on electron microscope in minimal change disease
podocyte damage
what is focal segmental glomerlosclerosis
fibrosis within the glomerulus
causes of focal segmental glomerlosclerosis
- Htn (esp African Americans)
- IV heroin abuse
- HIV
- reflux nephropathy
what is membranous nephropathy
thickening of the golmerulur basement membrane
how does membranou nephropathy usually present as
nephritic- nephrotic picture
-MC in Caucasian men >40 y/o
clinical manifestations of nephrotic syndrome
1) EDEMA (esp periorbital edema)
2) anemia
3) DVT
4) frothy urine
5) pulmonary edema
6) pleural effusion
Gold standard dx for nephrotic syndrome
24 hour urine protein collection
what is the diagnosis for nephrotic syndrome for a 24 hr urine protein collection
> 3.5g/day**
Diagnosis work up for nephrotic syndrome
- 24 hour urine protein collection
- UA
- Serum albumin/lipids
management of nephrotic syndrome: address these
- Minimal change dz
- FSGS
- edema reduction
- proteinuria
- hyperlipidemia
- Minimal change dz –> corticosteroids
- FSGS –> corticosteroids
- edema reduction –> diuretics
- proteinuria–> ACEI, ARB
- hyperlipidemia –> diet and meds
characteristic of UA of nephrotic syndrome
**oval fat bodies “maletese cross shaped”
what is acute glomerulonephritis
immunologic inflammation of the glomeruli causing PROTEIN** AND RBC** leakage into the urine
hallmark characteristics of glomerulonephritis
- HTN
- HEMATURIA (RBC CASTS)
- DEPENDEPENT EDEMA (PROTEINURIA)
- AZOTEMIA
name different etiologies of acute glomerular nephritis
- IgA nephropathy (Berger’s disease)
- Post infectious
- Membranoproliferative/mesangiocapillary
- Goodpasture’s disease
- vasculitis
which are etiologies of rapidly progressive glomerulonephritis (RPGN)
- Goodpasture’s disease
- Vasculitis
another name for IgA nephropathy
Bergers disease
what is the MC cause of acute glomerulonephritis in adults worldwide
IgA nephropathy
Pt usually presents with this type of AGN after a URI or GI infection, often affects young males within 24-48 hours
IgA nephropathy
how do you diagnose IgA nephropathy
+ IgA mesangial deposits
management of IgA nephropathy (Bergers disease)
ACE +/- corticosteroids
this type of AGN happens after GABHS
post infectious AGN
coca cola colored/dark urine
post infectious AGN
dx workup of post infectious AGN
- ASO titers
- Low serum complement (C3)
management of post infectious AGN
-supportive
how does membranoproliferative/mesangiocapillary AGN present
mixed nephritic /nephrotic picture
cresent formation on bx
rapidly progressive glomerulonephritis
management of RPGN
corticosteroids + cyclophosphamide
+anti-GBM antibodies
Goodpastures disease
dx of Goodpasture’s disease
linear IgG deposits
management of goodpasture’s disease
high dose corticosteroids* + cyclophosphamide* plus plasmapheresis
Microscopic polyangiitis dx
+ P-ANCA
granulomatosis w/ polyangiitis (wegnener’s) dx
+ C-ANCA
clinical manifestations of acute glomerulonephritis
- Hallmark- **hematuria (*coca colored/dark urine)
- Edema (85%): peripheral, periorbital (esp in children)
- Htn* (80%)
- *fever, abdominal pain, flank pain
management of Bergers disease/proteinuria
ACE inhibitors +/- corticosteroids
Tx of Lupus nephritis
steroids or cyclophosphamide
Tx for rapidly progressive AGN or severe disease
***corticosteroids PLUS cyclophosphamide
What happens in acute kidney injury in terms of creatinine and BUN
- increased serum creatinine >50%
- increased blood urea nitrogen/BUN (azotemia)
what is the most common type of AKI
pr-renal
what can prerenal AKI often lead to
acute tubular necrosis
what can prerenal AKI be caused by
reduced renal perfusion (hypovolemia)
examples of postrenal AKI
obstruction (BPH)
what type of AKI causes direct kidney damage
intrinsic
what causes intrinsic AKI
nephrotoxic, cytotoxic, prolonged ischemic
cellular cast formation
intrinsic AKI
what are the types of intrinsic AKI
- acute tubular necrosis (ATN)
- acute tubulointerstitial nephritis (AIN)
- glomerulur (acute glomerulonephritis-AGN)
what medications/ substances can cause nephrotoxic ATN
- *aminoglycosides, contrast dye, cyclosporine
- endogenous- crystal precipitation, myoglobuinuiria, lymphoma, leukemia
MC type of ATN
nephrogenic
muddy brown casts
acute tubular necrosis
epithelial cell casts
acute tubular necrosis
Labs values of K and Phosphate
- Hyperkalemia
- Increase phosphatemia
tx of AKI
- stop offending agent
- IV fluids
most causes of acute tubulointerstitial nephritis (AIN) is…
drug hypersensitivities
drug hypersensitivity that cause acute tubulointerstitial nephritis (AIN)
- PCNs*
- NSAIDs*
- Sulfa drugs*
- cephalosporins
- cipro
- rifampin
- allopurinol
clinical manifestations of acute tubulointerstitial nephritis (AIN)
- **fever
- *****esosinophila
- **maculopapular rash
- arthralgia
pathopneumonic UA from acute tubulointerstitial nephritis (AIN)
WBC CASTS, increased serum IgE
management of acute tubulointerstitial nephritis (AIN)
stop offending agent
tx for acute glomerulonephritis (AGN)
high dose corticosteroids
clinical manifestations of AGN
- *hematuria
- *HTN
- *azotemia
- *proteinuria
what are the two types of vascular AKI
- microvascular (TTP, HELLP syndrome, DIC)
- macrovascular (AA, renal artery dissection/thrombosis, malignant htn, atheroembolic disease-associated with ischemic digits/blue to syndrome esp. post cath, CABG or AAA repair)
Pre-renal AKI labs values:
- Creatinine
- Urine Na/FeNa
- UA
- Response to volume replacement
- BUN/Cr
- Creatinine: increases slower than 0.3mg/day
- Urine Na: <20 /FeNa: <1%
- UA: normal, HIGH specific gravity
- Response to volume replacement: *creatinine rapidly improves
- BUN/Cr: increased *>20:1
Acute tubular necrosis (ATN) lab values:
- Creatinine
- Urine Na/FeNa
- UA
- Response to volume replacement
- BUN/Cr
- Creatinine: increases AT 0.3-0.5 mg/dL/day
- Urine Na: >40 /FeNa: >2%
- UA: *epithelial cells, granular casts, LOW specific gravity
- Response to volume replacement: creatinine WONT improve
- BUN/Cr: 10-15:1
how is adult polycystic kidney disease inherited
autosomal DOMINANT
what is adult polycystic kidney disease
multisystemic progressive enlarged and formation of kidney cysts AND cysts in other organs
where can cysts from polycystic kidney disease be in other places of the body
- liver
- spleen
- pancreas
what does vasopressin stimulate to cause ESRD in polycystic kidney disease
cytogenesis
clinical manifestations of polycystic kidney disease
- abdominal/flank pain
- palpable flank mass
- HTN
- hematuria
what are EXTRArenal manifestations of polycystic kidney disease
- ****CEREBRAL BERRY ANEURYSMS
- ***MITRAL VALVE PROLAPSE
- *HEPATIC CYSTS
- *COLONIC DIVERTICULA
most widely used 1st dx for polycystic kidney disease
renal US
dx work up of polycystic kidney disease
- renal US
- CT scan/MRI (more sensitive than US)
management of simple AND multiple cysts in polycystic kidney disease
- simple: observation, ACE for htn
- multiple: supportive, *increase fluid intake (decreases vasopressin)
clinical manifestation of hypophophatemia
- DIFFUSE muscle weakness
- flaccid paralysis (due to decreased ATP)
clinical manifestations of hyperphosphatemia
- most asymptomatic
- heart block
- *soft tissue calcifications
what are the stages of CKD
stage 1: >90 w/ proteinuria/abnormal urine stage 2: 60-89 stage 3a: 45-59 stage 3b: 30-44 stage 4: 15-29 stage 5: <15 ESRD
what is the MC cause of ESRD
DM
what is the 2nd MC cause of ESRD
htn
single best predictor of renal disease progression
proteinuria
what is the best test to measure CKD
spot Ualbumin/Ucreatinine ratio (ACR)
what is the second best test to measure ckd
24 hour urine collection
broad waxy casts
ESRD
salt and pepper appearance of the skill on x-ray
osteitis fibrosis cystica
what is the biggest electrolyte abnormality is SIADH
hypOnatermia (becuase the blood is becoming diluted by the excess amount of water)
what is SIADH
excess increased in ADH causing the inability to dilute the urine (increases free water retention)
what is the MC cause of SIADH from CNS
stroke
what pulmonary ca can secrete ectopic ADH causing SIADH
small cell lung cancer
in isovolemic hypotonic hyponatremia is the serum osmolarity increased to decreased
DECREASED
is the urine osmolarity increased or decreased in SIADH
INCREASED
mainstay tx of SIADH
H2O restriction
how do you tx severe cases of SIADH that are refractory to H2O restriction
demecycline
why do you want to only correct hyponatermia no faster thatn 0.5mEq/L per hour
dont want to have central pontine myelinolysis
what is diabetes insipidis
inability of the kidney to concentrate urine –> large prodcution of DILUTE urine
central DI vs nephrogenic DI
central: decreased ADH production (MC type)
nephrogenic: partial or complete INSENSITIVITY to ADH
what is the MC type of DI
central
what are the MC manifestations of DI
- polydipsia
- polyuria
- nocturia
how do you dx DI
fluid deprivation test*
what is a + fluid deprivation test for DI
continued production of dilute urine
what test allows us to differentiate between nephrogenic and central DI
desmopressin (ADH) stimulation test
what would be the desmopressin test result of a central vs nephrogenic DI
central: reduction in urine output**
nephrogenic: NO reponse to desmopressin, continued urine output
tx for central DI
desmopressive/DDAVP or carbamazepine
tx for nephrogenic DI
HCTZ
