My Notes On Acute And Chronic Kidney Failure


My Notes On Acute And Chronic Kidney Failure

My Notes On Acute And Chronic Kidney Failure Peter  

5 years ago

~8.2 mins read
Kidney Failure

- A Rapid decline in Renal Fnx that persists for hours to less than a 3 month.
- Plus an increase in serum creatinine level (50% or 0.5-1mg/dL increase)
- Creatinine is normal in early stages ( becasue it takes time to accumulate)

Criteria for AKI (RIFLE)
FAILURE = 3x normal serum Creatinine, GFR < 50%
LOSS = Need dialysis > 4 weeks
ESRD = Need dialysis > 3 months

Taking note of duration of loss of kidney fnx in important to make a diagnosis

General Features in all Kidney Injury
- Weight gain and Edema (due to decreased Na+ excretion/accumulation)
- Azotemia (decreased excretion/increase absorption of ammonium compounds)

Edema (Excess fluid collection in cells) can only exist when
1. There is obstruction of flow
2. There is increased Na in ECF
3. There is decreased Albumin in ECF
4. There is increased Hydrostatic pressure

In general, there is decreased Excretion of metabolic waste either because the kidneys are trying to conserve volume by reducing filtration and secretion and Increasing reabsorption or because It has lost the function to Filter, to secrete.


Prognosis of Acute Kidney Injury (AKI)/Acute Kidney failure (depends on severity)
- >80% recover completely

Common cause of death in AKI
- Infection > Cardiorespiration complicatns

Types of AKI 
1. Pre-renal
- Due to decrease in Renal blood flow
- 70% cases (See a pt with AKI suspect Pre-renal first)
- Kidney function is perfectly at the time of diagnosis
- kidneys would reabsorb everything absorbable
- Kidneys would also reduce filtration and secretion capacity
- Pt would have signs of low BP

2. Intrinsic
- Due to damage to renal tissue = Loss of renal fnx
- Filtration ability is lost (Metabolites supposed to be filtered/Waste accumulate)
- Kidneys cant respond to hormones (esp. PTH, Aldosterone)
- Kidneys cant secrete metabolites (Waste accumulate, eg Uric acid)
- Kidneys cant reabsorb properly (esp. Albumin, BUN etc)
- Pick clues from a Pt if he may have had a recent RTI, Allergic reaction, Rash, Pre renal factors (Eg Hypotension)




- tract obstruction
- Pt may have a suprapubic mass

Pre-renal failure
Etiology/Risk factors
Caused by any condition that results in any of the following
1. Decreased Blood volume
2. Decreased Blood flow to kidenys
3. Decreased Blood Pressure

Summarise causes into 3D’s
1. Dehydration
2. Drugs (Diuretics, NSAIDS, ACE inhibitors, Cyclosporins, Anti-HTN)
3. Diseases (Sepsis causing vasodilation, Hepatorenal syndrome, conditions causing obstruction of renal vessels)

Pathophysio of Pre-renal AKI
1. Decreased RBF = Decreased GFR (to conserve volume) = Everything accumulates
(Any factor causing decreased blood flow to the kidneys, makes the kidneys think there is low blood volume and so they try to conserve volume.)
2. Pre-renal, if not attended on time = Intricnsic renal fail

Signs and Symptoms of Pre-renal AKI
Are basically what you find in hypovolemia
They affect the
1. Skin (Dry skin, poor tugur)

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Mucous (Dry mucous membrane)
3. Circulation - Hrt and Urine (Tachycardia, Hypotension, Anuria etc)

Pre-Renal AKI laboratory findings
1. Oliguria
- Kidenys try Preserving Volume)
2. Inc BUN-Cr ration >20-1
- Remember that everythng is increased as a rule but BUN > Cr.
- Kidneys reabsorbs everything it can to keep volume
- Kidneys can reabsorb BUN, but cant reabsorb Cr (Can only filter and secrete creatiinine)
- Cr accumulates because of reduced secretion and filtration but not to as much extent as BUN that can be reabsorbed.
3. Increased Urine Osmoliality (>500 mOsm/kg)
- As a rule, Both electrolytesa and water are decreased
- Fluid < Electrolytes in Urine because of ADH
- Because everything is reabsorbed, there is less free water in urine and alot of electrolytes compared to the volume of water in the urine.
- ADH secreted to absorb free water = Increased intravascular volume.
4. Decreased Urine Na+ (< 20mEq/L)
- Na+ is highly reabsorbed to draw water and maintain intravascular volume 
- FENa is <1%
5. Increased urine - Plasma cr ration (>40-1)
- As a rule, every substances in the Urine is decreased
- But Urine is more concentrated because of the amount of solute (Creatine inclusive) dissolved in the reduced volume of water
6. Bland urine segment ?
- Benign sediment seen in the urine
- No Cells present
Intrinsic Renal failure
- Loss of Kidney fnx (Everything is lost in urine)
- Kidneys cant respond to Hormones
- Can't filter, secrete or reabsorb properly 

- Glomerular fnx
- Tubular fnx

- Edema (Common in all kinds of Kidney failure)
- Signs and Symptoms of conditions that can cause kidney damage (eg Allergic reactions, PSGN, Long standing Pre-renal AKI)
- Signs and Symptoms of certain diseases that their treatments are nephrotoxic (E.g NSAIDS in Chronic pain, ACE Inhibitors in HTN, Aminoglycosides in Older pts with infection)

Lab findings in Intrinsic RF
1. Decreased BUN-Cr ratio (<20-1)
- As a rule, they are both increased due to reduced filtration and secretion (Loss of funtion) 
- BUN is increased more than Cr in all types of kidney failure.
- BUN is not as high as it is in Pre-renal due to loss of absorption capacity of the kidney


Increased Urine Na+ (>40mEq/L)

- FENa > 2% to 3%
- Kidneys cant reabsorb Na+
3. Decreased Urine Osmolality (<350mOsm/kg)
- Water lost is >> than solutes lost
- Kidneys can't respond to the effects of Anti-Diuretic Hormone
4. Decreased Urine-Plasma Cr (< 20-1)
- Because more more water in urine vs more cr in urine.
- Free water in Urine >> Anysolute in Urine
- Kidneys wont respond to ADH

Post-Renal failure
1. Least cause of AKI
2. Obstruction of of solitary kidney or  Bilateral Urinary Tract (eg Retroperitoneal fibrosis)
3. Decreased Urine flow = Increased tubular pressure (Backup of Urine in tubulus) = Decreased Hydrostatic pressure in Kidney vessels (decreased GFR)
4. Fnx is restored if obstruction is relieved b4 damage to kidney parenchyma (ATN)

Diagnosing AKI
Look for the corresponding abnormalities with the following tests
1. Blood tests
- Azotemia (BUN, Cr)
- Electrolyes (Na+)
- Albumin (Indicates Intrinsic failure
2. Urinalysis
- Protein (If present in Urine = Intrinsic Failure or Co-morbid condition)
- Urine sediment (if bland = Pre renal, if contains cells = Intrinsic renal)
3. Urine Chemistry
- Electrolytes
- Osmolality
- FENa+

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Urine culture
- If suspect Infection
5. Renal Ultrasound
- Size of kidneys
- Obstruction
6. CT scan
7. Renal biopsy
- detects parenchymal damge
8. Renal arteriography
- only If tx exits for arterial obstruction

In Pre-Renal
Everything that can be absorbed is high in serum
Everythijng filtered is high in serum and low in Urine due to less reaching the kidneys

In Intrinsic
Everything that is reabsorbed cant be absorbed because of function loss, so they are high in Urine
Also Evrything secreted is accumulated in the serum

Complications of AKI
- Mostly complications of Intrinsic Renal failure (worse prognosis)


Pulmonary Edema
- due to Inc Na+
- Dec. Albumin in Intrinsic
2. Metabolic complications (Hypo-CaN, Hypo-PUK)
- Hyperkalemia (Kidney wont respond to Aldosterone)
- Met. Acidosis ( H+ moves with K+, also H+ anf K+ are  normally secreted in exchange for reab of Na, so if )
- Hypocalcemia (kidneys dont respond to PTH)
- Hyponatremia (cant reabsorb Na)
- Hyperphosphatemia (Kidneys dont respnd to PTH)
- Hyperuricemia (Uric acid cant be secreted into tubules)
3. Uremia
- Uremia (Toxic end products of metabolism)
- kidneys cant secrete Urea
4. Infections
Most common cause is Uremia
Uremia causes immune dysfunction, if they were to exert pro-apoptotic effects, and increase the state of inflammation if they were to exert anti-apoptotic effects.)
- Pneumonia
- Wound infection
- sepsis

Treaten for AKI
A.  General concept
- Stop the cause (if any identified)
- Treat the consequences
- Avoid events that cause kidney failure/Injury

B. Specifics
1. PreRenal Treatment
- N/S to maintain euvolemia, esp if low blood vol)
- If US, Swan-Ganz monitoring for accurate accessment of Intravascular volume
2. Intrinsic
- if ATN, give supportive therapy
- If Oliguric, give furosemide
3. Postrenal
-  bladder catheter to decompress UT

Chronic Kidney Disease (CKD)
Very similar to AKI except in Duration
Any loss of fnx > 3 months
Usually GFR < 60mL/min 
Most common in Afro-Americans vs Caucasians

Causes (HOD)
- Diabetes, - HTN, Other kidney Injuries.


Diabetes (most common cause)
2. HTN (Most common cause of CKD after diabetes)
3. Chronic GN (Third most common)
4. Interstitial Nephritis
5. Polycystic KD
6. Obstructive Uropathy
7.  AKI causes
Note: Diabetes and HTN can also be caused by loss of kidney function. (It's either they caused loss of kidney function, or loss of kidney function caused them)

Complications of CKD 
Mostly due to the ff:
- Uremia
- Fluid imbalances
- Electrolyte imbalances
1. Cardiovascular
- Uremic Pericarditis (due to Inflammation in Uremic dysfnx), 
- HTN (due to Na+ accumulatn, also B-cell activation of the kidneys to decreased blood flow to kidneys)
- CHF (from volume overload, Secondary to Na+ retention)
2. GIT -
- Vomit, Anorexia (possibly due to hyperammonemia action?)
3. Neurologic effects - Asterixis, Seizures (hyperammonemia encephalopathy)


- Uremia,
- decreased production of red blood cells, 
- Loss of proteins and cells in urine
- proapototic effect on Uremia on immune cells
5. Endocrine
- Uremia
- Sexual (Hypothalamic - Gonadal dysfnx)
6. Electrolytes - k, po, ca, mg (hypo-CaN, Hyper-PUK)
7. Immune - Uremia immunocom

Diagnosing CKD
- take note of conditions that may signal kidney dysfnx
(E.g Rapid weight gain and Edema)
- CBC (Anemia, Thrombocytopenias)
- Renal US (Size of kidneys)
- Renal Biopsy

Treatment for CKD
1. Diet - Protein (0.7/0.8g/kg), Electrolytes balance
2. ACE inhibitors
- reduce risk of progression to ESRD
- Can cause hyperkalemia, be cautious
- Ironically, they can cause pre-renal failure
3. BP control (Treatment of cause or consequence)
4. Glycemic control if Diabetic (TX of cause or consequence)
5. Quit smoking
6. Correct electrolytes
- Hyperphosphatemia with Calcium citrate
- Long term oral calcium and vit D prevents 2o HyperPTH
- HCO3 replacement for Acidosis
- Erythropoietin for Anemia


Capsaicin cream or cholestyramine and UV light for Pruritus
8. Diuretics > dialysis for Pulmonary edema
9. Dialysis (when anuria)
10. Transplantation 
- only cure.
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