IM Acute Kidney Injury

Acute Kidney Injury

• Types:
  • Post: Stones, Cancer, or Prostate in Kidney, Ureter, or bladder
    
  • Pre: CHF/MI, Osi (cirrhosis, nephrosis, volume down, RAS/FMD
    
  • Intra: AIN, ATN, nephritic, nephrotic
    
  • Before calling nephrology: US, Urine lytes (Na, K, Cl, Cr, and Urea), UA w/micro, Spot protein
• Work-up:
  • increased serum creatinine >50%
    
  • an abrupt rise in creatinine or failed creatinine clearance
  • Requires 1 or more:
    • -increased serum creatinine
      
    • -reduced urine output
      
    • -need for renal replacement therapy
      
    • AND has to occur within 48 hours
  • -increased serum creatinine
    
    • look at PAST VALUES.
    • look at the RATE of the rise in creatinine-this will help determine if acute or chronic
  • -increased BUN
    
  • -urine sodium >20
    
  • -decreased GFR
  • FeNa
    • if FENa is <1% = prerenal cause of AKI
    • if FENa is >2% = intrinsic renal cause of AKI
    • Note: Pt taking diuretics will have inaccurate FeNa test
• 3 Criteria to grade AKI:
  • -rifle
  • -KDIGO
  • -AKIN
• Presentation:
  • Mild to moderate, typically asx
  • severe AKI:
    • -listlessness
      
    • -confusion
      
    • -fatigue
      
    • -anorexia
      
    • -NV
      
    • -weight gain
      
    • -edema
• Nephrotoxic Meds:
  • -NSAIDs
    
  • -abx
    
  • -acyclovir
    
  • -HIV
    
  • -iodinized radiocontrast meds
• Work-up:
  • UA:
    • -high specific gravity
      
    • -increased urine osmolarity
  • Renal US:
    • Use if concern for hydronephrosis
  • Bladder US:
    • Use to look for retention
  • Renal CT:
    • -to look for extrarenal causes of obstruction, like pelvic tumors
      
    • -renal lithiasis
      
    • -renal cancer
  • Renal Biopsy:
    • the gold standard to diagnose but not needed often.
    • needed to discover the cause of intrinsic AKI.
    • use when you need a specific dx based on the treatment plan.
• Treatment:
  • treat underlying cause prerenal, intrarenal or postrenal
  • Outpatient tx if reversible cause and can easily be fixed, or if the patient is amenable to close follow up

Pre-renal AKI

• Etiology:
  • -hypoperfusion, decreased perfusion to the kidneys-nephron is still structurally intact,
  • can lead to intrinsic injury if not corrected
     
• Causes:
  • -hypovolemia: renal volume loss due to diuretics, GI loss (diarrhea or vomiting), blood loss
  • -afferent arteriole vasoconstriction from NSAIDs, IV contrast==> this leads to decreased glomerular filtration
  • -efferent arteriole dilation from ACEI, ARBs
  • -hypotension
  •  -decreased CO
• Treatment:
  • Volume repletion (IVF) to restore volume and renal perfusion.
  • stop offending agents (like diuretics ACE/ARB/NSAIDs).

Post-Renal AKI

• Presentation:
  • -asymptomatic
    
  • -changes in urine output
    
  • -HTN
    
  • -rarely pain
  • Symptoms depend on:
    • -degree of obstruction
      
    • -rapidity of the obstruction (sudden complete obstruction vs more gradual partial obstruction)
• Causes:
  • characterized by the obstruction of the passage of urine
    
  • MC
    • men: enlarged prostate is the most common cause
      
    • women: pelvic tumor until prove otherwise
  • -tumors
    
  • -kidney stones
    
  • -bladder outlet obstruction (BPH, prostate cancer)
    
  • in general, this Is rare
• Work-up:
  • US – preferred imaging
    • to look for signs of obstruction 
    • looks for hydronephrosis, urethral dilation, bladder distention
• Treatment:
  • remove obstruction

Intra-Renal AKI

• Etiology:
  • -anything that hurts the kidney itself.
  • can be tubular, glomerular (nephritic or nephrotic), interstitial or vascular
• Causes:
  
  • –nephritic: IgA nephropathy, post-infectious (post-streptococcal), membranoproliferative, RPGN
  • -tubular: acute tubular necrosis-interstitial: interstitial nephritis
  • –nephrotic syndrome: minimal change, membranous neuropathy, focal segmental glomerulonephritis, diabetes mellitus
  • -vascular: thrombotic microangiopathy, atheroembolic renal disease 

Nephritic Vs. Nephrotic

• Hallmark:
  • nephrotic:
    • -proteinuria >3.5
    • -hypoalbuminemia
    • -edema
    • -hyperlipidemia
  • nephritic:
    • -proteinuria (<3.5)
    • -hematuria (+RBC casts)
    • -azotemia
    • -oliguria
    • -HTN
• Biopsy Finding:
  • nephrotic:
    
    • -hypocellular
  • nephritic:
    
    • -hypercellular
• Notes:
  • -heavy exercise
    
  • -gaining/losing muscle mass

Nephritic Syndrome (Acute Glomerulonephritis)

• Presentation:
  • edema + HTN + hematuria + RBC Casts/dysmorphic RBCs + proteinuria 1-3.5 g/day + azotemia
  • -hematuria (hallmark, cola-colored)
    
  • -edema (peripheral and periorbital)
    
  • -fever
    
  • -abdominal flank pain
    
  • -malaise
    
  • -oliguria
    
  • -HTN common
• Work-Up:
  • UA
    • -hematuria + RBC casts
      
    • -dysmorphic RBCs
      
    • -proteinuria (<3 usually, can get into nephrotic range)
      
    • -high specific gravity
      
    • -increased BUN and creatinine
  • Renal Biopsy
    • Gold standard, but it is often not needed

IgA nephropathy (bergers disease)

• Etiology:
  • Most common cause of acute glomerulonephritis
  • Most commonly affected:
    • -young males within days of URI/GI infection due to IgA immune complexes
      
    • -ages the 20s-30s
      
    • -white and east Asian MC
• Path:
  • IgA complexes deposit in the mesangium →alternate complement pathway activated →cytokines and macrophages released → glomerular injury → leading to RBCs in the urine (hematuria, hence nephritic)
• Presentation:
  • recurrent gross hematuria (cola-colored) with associated URI, HTN, usually affects children and young adults, diagnosed by kidney biopsy
  • can also be microscopic hematuria incidentally found on UA
• Work-Up:
  • Labs:
    • -↑ Creatinine
      
    • -↓ GFR
  • UA: hematuria, proteinuria
  • Renal biopsy – definitive dx
    • IgA mesangial deposits on immunostaining
• Treatment:
  • -ACEI
    
  • +/- corticosteroids
    
  • -BP control, supportive tx

Post-streptococcal glomerulonephritis

• Etiology:
  • MC in Population:
    • -developing countries
      
    • -bimodal age range: 5-12 and >60
      
    • -males>females
  • Occur:
    • -after group A strep
      
    • -10-14 days after skin (impetigo)
      
    • -10-14 days after pharyngeal infection
• Presentation:
  • Asymptomatic → Nephritic Syndrome
  • Red to brown urine (Coca Cola urine)
  • Proteinuria
  • Edema
  • HTN
  • ↑ Creatinine
  • Recent hx of strep pharyngitis (1-3 weeks)
  • Ex: 2-4 year old boy with facial edema up to 3 weeks s/p strep with scany, cola-colored urine (oliguria and hematuria)
• Work-up:
  • Labs:
    • -↑ Creatinine
      
    • -↓ GFR
      
    • -Complement levels are ↓ for the first 2 weeks
      
    • -positive strep culture
      
    • -↑ASO titers
  • UA:
    • -hematuria
      
    • -dysmorphic RBCs with or without RBC casts
      
    • -proteinuria, can reach levels of nephrotic syndrome
  • Renal Biopsy:
    • hypercellularity, increased monocytes, and lymphocytes, immune humps of IgG, IgM, C3
• Treatment:
  • -supportive +/- Abx
• Prognosis:
  • -clinical sx typically resolve in a week
    
  • -creatinine normalizes in 3-4 weeks
    
  • -hematuria takes 3-6 months
    
  • -Adults may develop lasting HTN, persistent proteinuria, and renal insufficiency

Rapidly progressive glomerulonephritis (RPGN)

• Etiology:
  • -severe glomerular injury, rapidly progressive loss of renal function, necrosis, and basement membrane breaks
• Causes:
  • any acute glomerulonephritis can present with it.
  • Goodpasture and vasculitis can ONLY present with RPGN
• Work-Up:
  • Renal Biopsy: crescents- due to fibrin and plasma protein deposition collapsing on the crescent shape of Bowmans capsule
• Treatment:
  • corticosteroids + cyclophosphamide

Goodpastures

• Work-Up:
  • Labs:
    • + anti-GBM antibodies

Henoch Schonlein Purpura (IgA Vasculitis)

• Etiology:
  • Immune complex-mediated, small vessel vasculitis
  • Population:
    • -kids ages <10 years, peaks at age 6
      
    • -it is seasonal, MC late fall to early spring
• Path:
  • IgA complexes are deposited in vessel walls, triggered by an antigen in a bacteria/virus, medication, or environmental factor → causes purpura, GI bleeding, hematuria
• Presentation:
  • Palpable purpura
    
  • Arthritis
    
  • Abdominal pain
    
  • Renal disease
• Treatment:
  • -supportive
    
  • -prednisone if renal involvement is severe

Acute tubular necrosis

• Etiology:
  • most common kind of intrinsic kidney injury
• Causes:
  • -due to toxic or ischemic injury to the nephron tubular epithelium
    
  • -can be caused by a few minutes to hours of ischemia
    
  • -prerenal AKI can also cause this
  • most likely following injection of radiocontrast dye
• Presentation:
  • -signs of dehydration, hypovolemia: tachycardia, dry mucous membrane, decreased skin turgor, cool extremities, orthostatic hypotension changes
    
  • -MC in hospitalized patients
• Questions to ask pt:
  • -hx of recent event that could have caused ischemia/hypovolemia: shock, sepsis, hypotension
    
  • -exposure to nephrotoxins
• Complications:
  • -electrolyte abnormalities
    
  • -acid-base abnormalities
    
  • -need for renal replacement therapy
    
  • -CKD
• Work-Up:
  • UA
    • -high creatinine (in less than 48 hours)
      
    • -FENa >2
      
    • -microscopic hematuria
      
    • -muddy brown, granular epithelial cell casts
      
    • -CBC
• Treatment:
  • -remove offending agent/determine cause
    
  • -no proven therapies to benefit ATN– use supportive management
    
  • -maximize volume status
    
  • -regulate hemodynamics
    
  • -watch and tx acid/base abnormalities
    
  • -avoid nephrotoxic meds
    
  • -dialysis

Interstitial Nephritis

• Presentation:
  • -fever
    
  • -maculopapular rash (urticaria)
    
  • -arthralgias
• MC cause:
  • -drug hypersensitivity:
    • esp NSAIDs and selective COX2 inhibitors, penicillin, sulfa drugs
      
  • -can also be due to associated infection or immune or neoplastic conditions
• Work-Up:
  • Labs
    • ↑ Creatinine
      
    • ↓ GFR
      
    • -eosinophils on CBC
  • UA
    • -WBC casts
      
    • -eosinophilia (think– because drug hypersensitivity reaction- IgE)
      
    • -proteinuria, pyuria, hematuria
• Treatment:
  • -remove the offending agent
    
  • -prednisone + supportive therapy
    
  • -most recover kidney function within a year

Nephrotic Syndrome

• Presentation:
  • the patient has peripheral or periorbital edema, ascites, pleural effusions, and hypertension. 
  • Proteinuria is > 3.5 grams per day (on 24-hour urine) 
  • lab tests show hypoalbuminemia and hyperlipidemia
  • -generalized edema
    
  • -frothy urine
    
  • -ascites and anasarca if severe
    
  • -anemia
    
  • DVT – loss of protein C, S and antithrombin, and liver producing more clotting proteins
• Types:
  • -minimal change
    
  • -membranous neuropathy
    
  • -focal segmental glomerulosclerosis
    
  • -diabetes mellitus (Most common secondary cause of nephrotic syndrome)
    
  • MC common cause of the nephrotic syndrome is idiopathic
• Rule of 3s for the idiopathic nephrotic syndrome:
  • describes the prognosis.
    
  • 1/3 get better, 1/3 stay the same, 1/3 worsen to CKI
• Work-Up:
  • UA
    • -proteinuria (leading to foamy urine)
      
    • -lipiduria
      
    • -microscopy: oval Maltese cross-shaped fat bodies (fatty casts)
  • 24-hour urine protein>3.5
    • Gold standard dx
• Treatment:
  • -Na and fluid restriction
    
  • -loops (edema reduction)
    
  • -ACE/ARB (reduce proteinuria)
    
  • -diet modifications/stains (reduce lipids)
    
  • -AC for VTE prevention is sometimes added

Minimal change disease

• Etiology:
  • most common nephrotic syndrome in children.
  • decrease in glomerular filtration, due to a decrease in osmotic pressure.
• Presentation:
  • -sudden onset edema and oliguria
• Work-Up:
  • UA
  • Renal Biopsy
    
    • -no visible changes on simple light microscopy
      
    • -podocyte damage seen on electron microscope
• Treatment:
  • -prednisone
    
  • -immunosuppressive medications
    
  • -eliminate nephrotoxic meds
    
  • -treat symptoms and complications

Membranous nephropathy

• Etiology:
  • most common cause of nephrotic syndrome in caucasian males under 40

Focal segmental glomerulosclerosis

• Presentation:
  • -HTN
    
  • -heroine
  • -HIV
    
  • -AAs
    
  • -obese
  • hematuria
    
     
• Treatment:
  • -ACEI
    
  • -prednisone
    
  • -immunosuppressants
• Prognosis:
  • poor prognosis depends on the degree of proteinuria

Membranous Nephropathy

• Treatment:
  • -moderate to high risk: glucocorticoids and cyclophosphamide
    
  • -low risk: ACEIs