AKI/CKD (burm)

4 Functions of the Kidney

1. regulate fluid-electrolytes

2. excrete waste

3. control BP

4. regulation of acid-base

Hormones that work in the kidney?

Parathyroid hormone

ADH

Aldosterone

What is AKI?

acute injury that manifests quickly and normally occurs because of an infection or inflammation

it can be small up to failure. can progress to CKD

What is CKD?

chronic kidney disease that manifests silently over years and normally develops as a result from long term diseases like DM/HTN

How do you characterize AKI?

abrupt reduction of kidney function commonly cuased by acute tubular necrosis

-presence of elevated BUN and SCr

What are the three classification systems for AKI and how does using them help patients?

1. RIFLE

2. AKIN criteria

3. KDIGO

-better identifications, diagnosis, and treatments

What are the three main etiologies of AKI?

1. Prerenal

2. intrinsic

3. Postrenal

Pathogenesis of postrenal AKI

obstruction within the kidney itself, bilateral ureter obstruction, urethral obstruction

RIFLE

Risk→ Injury→ Failure→ Loss→ End-stage kidney disease

uses SCr and GFR to measure

What are the two measures we use to determine level of kidney function?

GFR

SCr

SCr

product of muscle creatine metabolism

filtered by kidney but not reabsorbed

-used to measure GFR

Clearance rate=

UV/P

urine concentration x urine volume excreted

———————————————————————————

plasma concentration

Normal CrCl

125 mL/min

Different SCr levels and what happens when values double? Triple?

women- 0.7

men- 1.0

muscular men- 1.5

the amount it increases is how much function you subtract form normal function (double= 50% function; triple= 25% function

Two main causes of pre-renal AKI

1. decrease blood flow to kidney (hypovolemia)

2. decrease effective arterial blood volume (shock)

RBF is regulated by

CO

renal perfusion pressure

glomerular hemodynamic factors

autoregulation

Pathogenesis of Prerenal AKI

-60% of all AKI

-Reduced blood flow to the kidney

-reversible

-increased BUN and SCr

-oliguria

-

What response occurs because of intravascular volume depletion (decreased RBF)?

RAAS and SNS activation

CM of pre-renal AKI

↓ urine Na+

↓ excretion of Na+

↓ excretion of urea

↓ urine output

↑ urine osmolarity

↑ urine specific gravity

How do you prevent prerenal AKI?

correct and prevent hypovolemia

Pathogenesis of intrinsic AKI

direct damage of glomeruli, tubules, interstitium, or blood vessels

-increase in BUN and SCr

-doesn't always bounce back

What are the causes of intrinsic AKI?

vasculitis, acute glomerulonephritis, acute interstitial nephritis, acute tubular necrosis, sepsis, ischemia, untreated pre-renal AKI

inflammation of interstitial tissue of the kidney

-normally a reaction to a medication (penicillin, NSAIDs, PPI)

-presents as allergic reaction

-need a renal biopsy to diagnose

Acute interstitial nephritis

Two types of glomerulonephritis

Acute

rapidly progressive

-IgA nephropathy

-20-30 y/o

-gross microscopic hematuria

-deposition of IgA

-formation of crescents

-managed with blood pressure and DLD meds

Acute glomerulonephritis

-due to postinfectious glomerulonephritis

-can cause CKD if you have goodpasture syndrome

-extensive necrotic crescent formations

-serologic tests to identify

rapidly progressive GN

What are the types of Acute tubular necrosis (ATN)?

1. ischemic

2. nephrotic

3. contrast-induced nephropathy

4. sepsis-induced

-prolonged hypoperfusion

-loss of autoregulation whihc enhances vasoconstriction

-type of ATN

Ischemic ATN

Progression to an ATN

injury → increase vasoconstriction/decrease vasodilation → decrease in RBF → decrease in perfusion → decrease GFR

-direct toxic damage

-caused by meds or hemolysis

-nephrotoxic agents have accumulated in the cortex

nephrotoxic ATN

-significant cause of ATN

-caused by IV radiocontrast agents

-it is mostly hospital acquired

contrast-induced nephropathy

-70% mortality rate

-most common AKI in hospital

-can be caused by ischemia, toxic damage, endotoxin, sepsis

sepsis-induced ATN

What can happen if you do not recovery from intrinsic AKI?

CKD or ESRD

T/F: AKI and CKD are dependent of each other.

False

they can both occur as a result of each other, but they also can occur independently of each other

What are the three phases of an AKI?

1. initial

2. maintenance

3. recovery

Initial phase of intrinsic AKI

-changes in urine output/ increase SCr

-may be nonoliguric

-time from injury to reduction in renal function

Maintenance phase of intrinsic AKI

- 2-8 weeks

-SCr rises more

-oliguria or anuria or normal

-edema (peripheral and pulm) if oliguric

Recovery phase of intrinsic AKI

3-12 months

SCr normalizes

-polyuria

-fluid and electrolyte abnormalities

How does our sodium/water levels change in a prerenal and intrinsic AKI?

pre= less sodium and water excretion (osmolarity increases)

intra= more sodium and water excretion (osmolarity decreases)

What is looked at during an urinalysis?

urine [Na+]

urine FEna+

urine FEurea

difference in FE na+ in Pre and intra renal AKI

pre= below 1%

intra= above 2%

difference in FE urea in Pre and intra renal AKI

pre= below 35%

intra= above 50%

What is the common cause of postrenal AKI?

obstruction of the urinary collecting system

-either kidney stones, bilateral ureteral, other

CM of complete obstruction postrenal AKI

anuria

sudden cessation of urine

hydronephrosis (swelling)

CM of partial obstruction postrenal AKI

frequency, hesitancy, nocturia, incomplete emptying of the bladder

renal colic, pelvic fullness, hematuria, flank pain

Define CKD

GFR < 60 mL/min for 3+ months

Modifiable risk factors of CKD

DM, HTN, DLD, obesity, AKI hx, protein and sodium intake

KDOQI

Kidney Disease Outcomes Quality Initiative

-help with the identification, prevention, and treatment of CKD

What are the four main causes of CKD?

1. diabetic nephropathy

2. HTN nephrosclerosis

3. chronic glomerulopheritis

4. polycystic kidney disease

-most frequent cause of CKD

-occurs in diabetic patients

-indicated early by albuminuria

-due more to hyperglycemia instead of hypo

diabetic nephropathy

-a cause of CKD

-increase incidence of ESRD

-more in AA

-impaired renal autoregulation

-increase pressure in glomerulus, damage to small vessels, compensatory hyperfiltration by undamaged nephrons

Hypertensive nephrosclerosis

-cause of CKD

-direct inflammation of glomerulus (antibody deposition)

-leads to tubular and glomerular fibrosis

-chronic (more over time)

-nephritic vs nephrotic pattern

-requires a renal biopsy to diagnose

chronic glomerulonephritis

Nephritic vs nephrotic

I= w/ inflammation, active urine sediment

O= w/ proteinuria, inactive urine sediment

-cause of CKD

-mutation in the PKD1 gene

-onset at 30

-develops on the collecting duct

polycystic kidney disease

complications of CKD

1. CKD-MBD

2. Anemia

3. CVD

4. HTN

5. DLD

6. Metabolic acidosis

7. Hyperkalemia

8. Hypervolemia

9. uremia

-Complication of CKD

-mineral and hormonal change

-in stage 3

-bone pain, deformities, fractures

-hypocalcemia, hyperphosphatemia, hyperparathyroidism

-bone and PTH becomes less responsive

CKD MBD

mineral and bone disorder

-complication of CKD

-decreased EPO production

-increase preload, decrease afterload, increase CO

-LV hypertrophy and dilation

anemia

-most common cause of death in CKD

CVD

-can be a complication or a cause of CKD

-poor prognosis

HTN

-complication of CKD

-early onset

-the proteinuria of CKD can exacerbate this

DLD

-complication of CKD

-kidney retains H+ ions

-prominent in stage 4 and 5

-increase excretion of ammonia and retention of H+ ions

-decrease reabsorption of bicarb

metabolic acidosis

-complication of CKD

-increases as oliguria develops

-because of decreased aldosterone secretion

-associated with arrhythmias and hemodynamic instability

hyperkalemia

-complication of CKD

-decrease excretion of Na+ and water

hypervolemia

-complication of CKD

-can cause gi disturbances, CNS manifestations, edema, skin changes, worsening of metabolic acidosis, F/N/V/HA

-caused by waste product accumulation

uremia

non-Pharmacological treatments of CKD

hemodialysis

peritoneal dialysis

kidney transplant