CKD part 2 Flashcards
what is included in the nephritic spectrum
- urine sediment with hematuria, +/- RBC casts
- Proteinuria (< 3 g/d)
- Nephritic - i for inflammation/immune, which is often involved
what is included in the nephrotic syndrome
- “Bland” urine sediment - no cells or casts (May see oval fat bodies)
- Proteinuria (at least 300 mg/d, often > 3 g/d)
- Nephrotic - o for protein
- hypertriglyceridemia/hyperlipidemia
what are general findings of glomerulonephritis
- decreased GFR
- edema and HTN
- smoky/coca cola colored urine (hematuria)
- uremic s/s
lab findings in glomerulonephritis
- high serum Cr
- hematuria and protein in urinalysis
- RBC, WBC, RBC casts on urine sediment
I skipped all of the causes because we learned these in AKI
sorry:(
what is treatment for glomerulonephritis
- management of HTN and volume overload
- ACE/ARB for proteinuria
- immunosuppressive agents (high dose corticosteroids or cytotoxic agents)
- plasma exchange for goodpasture or pauci-immune glomerulonephritis.
what is postinfectious glomerulonephritis
glomerulonephritis due to bacteria or pathogens. usually GABHS
what test helps make the definitive diagnosis for postinfectious glomerulonephritis
biopsy showing “humps” of immune complex deposits.
what is the treatment for postinfectious glomerulonephritis
- treat infection
- supportive (antiHTN, diuretics, salt restriction)
- NO steroids (doesnt show improvement)
what is the MC primary glomerular disease worldwide
IgA nephritis (Berger’s Disease)
what is the demographics MC in Berger’s disease
2-3x more common in males; MC in children and young adults
what is the MC symptom in berger’s disease
Episode of gross hematuria.
(often in onjunction with URI)
what is considered low risk bergers disease and how would you treat it?
no HTN, normal GFR, minimal proteinuria
tx: monitor yearly
what is considered high risk bergers disease and how would you treat it?
proteinuria>1.0, decreased GFR, HTN
tx: ACE/ARB
what is the prognosis for bergers disease
33% spontaneous remission
20-40% progress to ESRD (especially if > 1 g/d proteinuria)
what is Henoch-Schonlein purpura
systemic small-vessel vasculitis assicaited with IgA deposition in vessel walls
what is the S/S of henoch schonlein purpura
- palpable purpura in LE and buttocks
- arthralgias
- abdominal symptoms (nausea, colic, melena)
what is the treatment for henoch schonlein purpura
no tx only supportive care (hydration, rest, sleep)
what is prognosis for henoch scholein purpura
make full recovery over several weeks. may progress to CKD
what is pictured
henoch scholein purpura
what is the MCC of nephrotic glomerular disease in US
DM
what are the general S/S of nephrotic syndrome
subnephrotic proteinuria - little to no s/s
nephrotic syndrome (peripheral edema, dyspnea, pleural effusions, ascites)
what does urinalysis show in nephrotic syndrom
proteinuria 300mg/d or more
what is the urine sediment showing in nephrotic syndrome
- If marked HLD - oval fat bodies
“Grape clusters” (light microscopy) or “Maltese crosses” (polarized light)
what do serum labs show for nephrotic sydrome
hypoalbuminemia (<3)
hypoproteinemia (<6)
hyperlipidemia
elevated ESR
possible Vit D, zinc and copper deficiency
what is the pathophysiology of hyperlipidemia in nephrotic syndrome
- Low protein → Low oncotic pressure → increased hepatic lipid production
- Lower clearance of VLDL → hypertriglyceridemia
What is the treatment for protein loss in nephrotic syndrome
- if mild decrease intake
- if severe (>10g/day) increase protein
- ACE/ARB to lower urine protein excretion
what is the treatment for edema in nephrotic syndrome
- dietary salt restriction
- thiazides and loops are protein bound so larger doses would be needed
what is the treatment for hyperlipidemia in nephrotic syndrome
diet and exercise, lipid lowering drugs
what is the treatment for hypercoagulability in nephrotic syndrome
anticoagulation for 3-6 months minimum if evidence of thrombosis.
Continue if renal vein thrombosis, PE, or recurrent thromboemboli
at what protein level is hypercoagulability usually seen in nephrotic syndrome
serum albumin <2g/dL
what is the MCC of proteinuric renal disease in children
minimal change disease in children (80%)
(this makes up 20-25% of proteinuric renal disease in adults)
what are s/s of minimal change disease
full blown nephrotic syndrome:
- thromboembolic events
- hyperlipidemia
- protein malnutrition
what is treatment for minimal change disease?
corticosteroids - specifically prednisone
for up to 8 weeks in children and 16 weeks in adults. taper off when done.
RARELY progresses to ESRD
what is the MCC of primary nephrotic syndrom ein adults
membranous nephropathy due to immune complex deposition
nephrotic syndrome could also be secondary to carcinoma, HBV, HCV, syphilis, endocarditis, autoimmune disease, NSAIDs, captopril
what are the s/s of membranous nephropathy
may be asymptomatic or may see edema and frothy urine.
what is treatment for membranous nephropathy
ACE/ARB, immunosuppression, transplant.
50% progress to ESRD
30% spontaneous remission
what is amyloidosis
extracellular deposition of amyloid protein
what are s/s of amyloidosis
- proteinuria, decreased GFR, nephrotic syndrome
- enlarged kidneys
- s/s of other chronic inflammatory disease
what is the treatment for amyloidosis
- manage underlying disease
treatment options are limited and 5 year survival rate is <20% :( sad day
what is the MCC of ESRD in the US
diabetic nephropathy!
20 year risk - 40% (higher risk in T2DM)
how does diabetic nephropathy present
developes about 10 years after DM onset
- early - hyperfiltration with increased GFR
- Later - microalbuminuria (30-300 mg/d)
- Progression - albuminuria 300+ mg/d
what is the treatment for diabetic nephropathy
- strict glycemic control
- treat HTN to goal - ACE/ARB can be used
What is tubulointerstitial disease?
disorder affecting renal tubules and interstitium (glomeruli and renal vessels not generally affected)
what is the main pathology of acute tubulointerstitial disease
acute interstitial nephritis
what are the main pathologies of chronic tubulointerstitial disease
interstitial fibrosis
tubular atrophy
what is the main cause of acute interstitial nephritis
70% due to medication
What are the causes of chronic tubulointerstitial disease
Obstructive uropathy (1st MCC)
vesicouretal reflux (2nd MCC)
analgesic nephropathy (1g/day 3+ yrs)
Autoimmune interstitial nephritis
nephrocalcinosis
can also be:
renal ischemia
glomerular disease
but we dont really go into these i dont think
what is obstructive uropathy
prolonged obstruction of the urinary tract leading to backflow of urine, movement of fluid into interstitium and then inflammation and fibrosis
this leads to damage and scarring
what are causes of obstructive uropathy
enlarged prostate
renal calculi
cancer
retroperitoneal fibrosis or mass
what are the s/s of obstructive uropathy
hydronephrosis
pain
bladder distension
HTN
Urine - oliguria, anuria or polyuria :/
what is hydronephrosis
this picture was just good for my brain to make sense of it.
what do UA and serum creatinine show in obstructive uropathy
UA - benign, may see hematuria or pyuria
serum Cr - elevated
what is the preferred imaging of study for obstructive uropathy and what does it show
US - may show dilation of collecting system.
only use CT if suspected stone!
how do you treat obstructive uropathy
relieve obstruction ASAP
if not removed quickly could lead to tubular damage and renal scarring
what is vesicouretal reflux disease and who is it MC in
primarily occurs in children
incompetent or misplaced vesicouretal sphincter leads to retrograde flow of urine while voiding.
this causes inflammatory responses and scarring
what is the presentation of vesicouretal reflux disease
- frequent UTIs (esp in children)
- may not be dx until later in life when HTN and proteinuria develope:(
what do labs show in vesicouretal reflux disease
- varying elevations in BUN/Cr
- mild-mod proteinuria
what imaging modalities can be used to assess vesicouretal reflux disesae
- voiding cystourethrogram (dye instilled in bladder, pt pees while xray is taken)
- US to assess for hydronephrosis and renal scarring
what would a US show in vesicouretal reflux disease
- hydronephrosis and renal scarring
Adults -
- asymmetric small kidneys
- irregular outlines
- thin cortices
- areas of compensatory hypertrophy
how do you describe dilation of the kidneys
idk if we need to know this tbh
how do you treat vesicouretal reflux disease
- maintain sterile urine in children
- surgical implantation of ureters (for children with persisten high grade reflux, NOT for adolescents or adults)
- control of HTN with ACE/ARB
what is analgesic nephropathy
tubulointerstitial inflammation and papillary necrosis in patients who ingest at least 1g/day of analgeics for 3+ years
what is the highest associated analgesic with analgesic nephropathy? what are some other common analgesics?
phenacetin!
may also be caused by:
NSAIDS, aspirin, tylenol!
why do analgesics cause papillary necrosis.
Analgesics can be concentrated up to 10x higher in renal papillae than in renal cortex
what is seen in urine of analgesic nephropathy
hematuria
proteinuria
polyuria
pyuria
sloughed papillae!!
what are image findings in analgesic nephropathy?
CT - small, scarred kidney with papillary calcifications
IVP - contrast will fill area of sloughed papillae, causing a “ring shadow” or “golfball on a tee” sign
NOTE: IVP rarely used d/t risk of constrast nephropathy
how do you treat analgesic nephropathy
discontinue analgesics
what is the cause of autoimmune interstitial nephritis
a combination of multiple autoimmune disorders as seen below!
what are clinical findings of autoimmune interstitial nephritis
- could be asymptomatic ¯_(ツ)_/¯
- polyuria
- volume depletion d/t salt wasting
- hyperkalemia
- hyperchloremic metabolic acidosis
what does immaging show in autoimmune interstitial nephritis.
small, scarred kidneys
what is the treatment for autoimmune interstitial nephritis
control underlying cause
what is nephrocalcinosis
deposition of calcium in renal parenchyma and tubules
what isthe prognosis of neophrocalcinosis
- Can cause AKI, CKD
- May also have normal renal function
- Most pts do not progress to ESRD
what is the cause of nephrocalcinosis
increased in urinary excretion of calcium (MCC), phosphate and/or oxalate
what is a risk factor for nephrocalcinosis
conditions that cause hypercalcemia, hyperphosphatemia or increased excretion of Ca, PO, or oxalate in urine
such as:
- hyperparathyroidism
- vit D therapy
- loops
what are lab findings in nephrocalcinosis
- hypercalcemia and hyperphosphatemia
- urine with sterile pyuria or hematuria
- proteinuria
- 24 hour urine may show increase Ca, PO or oxalate
what are s/s of nephrocalcinosis
usually asymptomatic, often found incidentally
what is the treatment for nephrocalcinosis
correct underlying metabolic disorder
what makes up 65-70% of all renal masses
single or solitary renal cysts, generally found in the outer cortex or medulla.
what is the management of a single or solitary renal cyst
if benign then routine follow up is acceptable.
refer to bosiak score for whether or not a cyst is benign!:)
what could a cyst developing after onset of dialysis suggest
potential for adenocarcinoma
what are the two types of cystic kidney disease and what causes them?
- juvenile nephronophthisis (in children) - autosomal recessive gene
- Adult medullary cystic kidney disease - autosomal dominant gene
what is the result of jevenile NPH and adult MCKD
multiple small renal cysts at corticomedullary junction and in medulla.
what are the s/s of medullary cystic kidney disease
polyuria, pallor, lethargy, renal salt wasting
later in disease:
HTN, hyperuricemia, growth restriction in juvenile NPH
what ages does ESRD occur in juvenile NPH and in MCKD
Juvenile NPH - <20 years
MCKD - ages 20-70
what is the treatment for medullary cystic kidney diseases
- adequate salt and water intake
- no therapy known to stop progression
- allopurinol if hyperuricemic
- does not recur in renal transplants.
what is the cause of Autosomal Dominant polycystic kidney disease
mutation of genes ADPKD-1 or ADPKD-2 via autosomal dominant inheritance (90%) or spontaneous mutation (10%)
what gene is more severe and more common in ADPKD
ADPKD-1 - 85% of patients.
ADPDK-2 15% of patients with slower progression and later onset in life.
what are s/s of ADPKD
- abdominal pain
- flank pain
- hx of UTI
- hx of HTN in >50% of patients
- family hx of PKD in 75%
- enlarged palpable kidneys!
what will labs show in ADPKD
hematuria and proteinuria
H&H is normal
what confirms the diagnosis of ADPKD
US showing:
- Age < 30 - 2+ renal cysts
- Age 30-59 - 2+ cysts in each kidney
- Age 60 + - 4+ cysts in each kidney
where else might cysts be seen in ADPKD
- liver
- spleen
what is the cause of pain in ADPDK? how do you treat it
cause - infection, bleeeding, nephrolithiasis
tx - bed rest, analgesics, cyst decompression
what is the cause of hematuria in ADPKD? How do you treat it?
Cause - MC due to rupture of cyst but could be Kidney stone, UTI
tx - bed rest, hydration, resolves in 1 week.
what could recurrent hematuria in ADPKD mean
possible renal cell carcinoma
How do you treat nephrolithiasis in ADPKD
pain control
hydration of 2-3L/day
how do you treat HTN in ADPKD
- ACE/ARB preferred
- cyst decompression
how does an infected cyst present in ADPKD and how do you treat it
presents with flank pain, fever and increased WBC
- cultures (blood and urine)
- TX with cystic penetration ABX
and continue with 2 weeks of IV ABX and long term oral ABX
what are other complications that can occur with ADPKD
- Cerebral aneurysms on circle of willis
- mitral valve prolapse
- aortic aneurysms
- aortic valve disease
- colonic diverticula
How do you treat ADPKD Cyst growth
- vasopressin receptor antagonists (slow progression)
- ocreotide ( decreased cyst growth)
- tolvaptan (slows renal decline)
what drug class is tolvaptan
vasopressin V2 receptor antagonist
when is tolvaptan recommended in ADPKD
in all patients 18+ with GFR of 25+ and 1+ risk marker which includes:
1. mayo class 1C, 1D, 1E
2. age <55 and eGFR <65
3. kidney length >16.5 cm in patient <50 y/o
4. PROPKD score of >6
what may help and/or slow progression of ADPKD
avoidance of caffeine
tx of HTN and proteinuria
How does tolvaptan aid in treatment of ADPKD
reduces urinary osmolality which impairs cyst growth
what are SE of tolvaptan
thirst
polydipsia
polyuria
nocturia
hypernatremia!!
increased liver enzymes
BBW!!! - should be initiated and reinitiated only in a hospital where serum sodium can be CLOSELY monitored!
what are CI for tolvaptan
liver disease
pts on strong CYP3A4 inhibitors
allergy
How does Autosomal recessive PDK present
- enlarged tubules with small cysts on collecting tubules only
- impaired urine concentration
- metabolic acidosis
- HTN common
what is the MCC of death in autosomal recessive PKD
pulmonary hypoplasia due to oligohydramnios (amniotic fluid abnormality)
what age do people with autosomal recessive PKD tend to live until? what complications will they have?
- 80% of surviving neonates live to 10 or longer
they will have complications such as:
- 1/3 with ESRD by 10
- portal HTN
- periportal fibrosis
what is the diagnosis for autosomal recessive PKD
large echogenic kidneys with cysts visible after birth.
absence of renal cysts in either parent confirms or denies ARPKD
what is treatment for ARPKD
manage HTN
dialysis
kidney transplant
what is the MCC of renal artery stenosis? what is the only other cause we learned?
80-90% d/t atherosclerotic occlusive disease
10-15% - fibromuscular dysplasia
when would you suspect fibromuscular dysplasia
unexplained HTN in woman <40
what are risk factors for RAS
HTN
atherosclerosis
CKD
DM
Tobacco use
what are the s/s of RAS
HTN
pulmonary edema
AKI after starting ACEI
may present with abdominal bruits!
what labs are seen in RAS
elevated BUN/Cr if significant ischemia
what does US reveal in RAS
asymmetric kidneys if unilateral or small hyperechoic kidneys if bilateral
what would an MRA reveal in RAS
turbulent blood flow with false positive results
what is the gold standard for RAS diagnosis
renal angiography
How do you treat RAS
- manage HTN
- angioplasty (reduces HTN meds needed but doesnt slow disease)
- surgical bypass (risky and not better than angioplasty)
what is nephrosclerosis
hypertensive nephropathy leading to sclerosis of arteries and arterioles. also causes interstitial fibrosis and decreased glomerular tuft!
what are risk factors for nephrosclerosis
African American race - 5x more common
Increased age, smoking, hypercholesterolemia
Longstanding uncontrolled HTN
what is treatment for nephrosclerosis
management of HTN with mulitple anti-HTN
thiazides and ACE/ARB are MC
what is cholesterol atheroembolic disease
emboli to kidneys usually d/t cholesterol crystals breaking free of vascular plaque and lodging in downstream microvessels
when might you see cholesterol atheroembolic disease
vascular surgery
trauma
heparin use
thromoblytic use
what are risk factors for cholesterol atheroembolic disease
male
DM
HTN
ischemic cardiac disease
what are the s/s of cholesterol atherembolic disease
onset 1-14 days after inciting event
- worsening HTN and renal function with fever, abdominal pain and wt loss.
may also see livedo reticularis and localized gangrene!
what labs are seen in cholesterol atheroembolic disease
increased Cr
eosinophilia
elevated ESR
low complement
what is definitive diagnosis for cholesterol atheroembolic disease
kidney biopsy
what is treatment for cholesterol atheroembolic disease
no specific effective therapy but can use:
- statins
- steroids (contraversial)
- supportive
oh ma lort that was a lot good luck yall
byeeeeeeee
