The document discusses acute renal failure (also known as acute kidney injury) and chronic kidney disease (CKD), detailing their causes, symptoms, and treatment options. It describes acute kidney injury as a sudden decline in kidney function due to prerenal, intrarenal, or postrenal factors, while chronic kidney disease is a progressive and irreversible loss of kidney function due to conditions like diabetes and hypertension. Various treatment strategies, including medication, dietary management, and renal replacement therapy, are highlighted to manage these kidney disorders.

1. Mrs. Babitha K Devu
Assistant Professor
SMVDCoN

2. Acute renal failure/ Acute Kidney Injury
Chronic renal failure/ ESRD

3. Introduction
also known as is
the partial or complete impairment of kidney
function. It result in an inability to excrete
metabolic waste products and water, and it
contributes to disturbances of all body system.
• The terms and renal failure
are used synonymously. The term uremic
syndrome describes a set of manifestations
that result from loss of renal function.

4. • Acute kidney failure occurs when your kidneys
suddenly become unable to filter waste
products from your blood. When your kidneys
lose their filtering ability, dangerous levels of
wastes may accumulate, and your blood's
chemical makeup may get out of balance.

5. Acute kidney injury is a syndrome characterized by:
• Sudden decline in GFR (hours to days )
• Retention of nitrogenous wastes in blood
(Azotemia)
• Disturbance in extracellular fluid volume and
• Disturbance in electrolyte and acid base
homeostasis

6. The causes of AKI, which are multiple and complex,
are categorized as:
Prerenal
Renal/ Intrinsic
Postrenal

7. Prerenal: These causes of AKI are factors external to the
kidneys.
Hypovolemia
Dehydration
Hemorrhage
GI losses (Diarrhea, Vomiting)
Excessive diuresis
Hypoalbuminemia
Burns

8. Prerenal: These causes of AKI are factors external
to the kidneys.
Decreased cardiac output
Cardiac dysrhythmias
Cardiogenic shock
Heart failure
MI

9. Prerenal: These causes of AKI are factors external to
the kidneys.
Decreased peripheral vascular resistance
Anaphylaxis
Neurologic injury
Septic shock
Decreased renovascular blood flow
Bilateral renal vein thrombosis
Embolism
Hepatorenal syndrome
Renal artery thrombosis

10. IntraRenal/ Intrinsic
Nephrotoxic injury
Drugs: Aminoglycosides
Contrast media
Hemolytic blood transfusion reaction
Severe crush injury
Chemical exposure
Interstitial Nephritis
Allergies
Infections: Bacterial, viral, fungal

11. IntraRenal/ Intrinsic
Other causes
Prolonged prerenal ischemia
AGN
Thrombotic disorders
Toxemia of pregnancy
Malignant HTN
SLE

12. Postrenal
BPH
Bladder Cancer
Calculi formation
Neuromuscular disorders
Prostate cancer
Spinal cord disease
Strictures
Trauma

13. • Being hospitalized, especially for a serious condition that
requires intensive care
• Advanced age
• Blockages in the blood vessels in your arms or legs
(peripheral artery disease)
• Diabetes
• High blood pressure
• Heart failure
• Kidney diseases
• Liver diseases

14. Due to the etiological factors
Reduced systemic circulation, causing a
reduction in renal blood flow.
Decreased glomerular perfusion and GFR
(But no damage to the kidney tissues)
Prerenal Azotemia

15. When there is a decrease in circulating blood
volume, autoregulatory mechanisms increase
angiotensin II, aldosterone, norepinehrine and
ADH as an attempt to preserve blood flow to
essential organs.
If the causes are not corrected, the decreased
perfusion persist, the kidney lose their ability to
compensate and damage to kidney parenchyma
occurs (intrarenal damage).

16. Due to the intrarenal causes
Direct damage to the kidney tissues from prolonged
ischemia, nephrotoxins, hemoglobin released from
hemolyzed RBCs, or myoglobin released from necrotic
muscle cells.
Impaired nephron function due to damage to the
epithelial cells of the tubules or Hb/myoglobins can
block the tubules or infections can damage GBM

17. Postrenal causes of AKI involve mechanical
obstruction in the outflow of urine
Urine refluxes into the renal pelvis leads to
hydronephrosis, increase in hydrostatic pressure
and tubular blockage.
Progressive decline in kidney function

21. A thorough history collection for diagnosing etiology.
Physical examination:
Serum Creatinine and BUN levels
Serum electrolytes
Urinalysis
Renal USG
Renal scan
CT scan/MRI
Renal biopsy

22. Fluid buildup. Acute kidney failure may lead to a
buildup of fluid in your lungs.
Chest pain.
Muscle weakness.
Permanent kidney damage.
Death. Acute kidney failure can lead to loss of
kidney function and, ultimately, death. The risk of
death is higher in people who had kidney problems
before acute kidney failure.

23. Goals of treatment for AKI
Eliminate the cause,
Manage the signs and symptoms, and
Prevent complications while the kidneys recover.

24. Determine is there adequate intra-vascular
volume and cardiac out-put to ensure adequate
perfusion of the kidneys.
Treatment for acute kidney failure involves
identifying the illness or injury that originally
damaged your kidneys. Your treatment options
depend on what's causing your kidney failure.

25. IV fluids if the renal failure is due to fluid loss.
Diuretics is often administered but not
recommended in high doses. Loop diuretics
(furosemide [Lasix], bumetanide [Bumex]) or an
osmotic diuretic (mannitol).
If AKI is already established, forcing fluids and
diuretics will not be effective and may, in fact, be
harmful.

26. Closely monitor fluid intake during the oliguric phase
of AKI.
The general rule for calculating the fluid restriction -
Add all losses for the previous 24 hours (urine,
diarrhea, emesis, blood) plus 600 mL for insensible
losses (respiration, diaphoresis). For example, if a
patient excreted 300 mL of urine on Tuesday with no
other losses, the fluid allocation on Wednesday
would be 900 mL.

27. Therapies for elevated Potassium Levels:-
Insulin and na+ bicarbonate serve as a temporary
measure for treatment of hyperkalemia by promoting
a shift of potassium into the cells, but potassium will
eventually be released.
IV glucose is given concurrently to prevent
hypoglycemia. When effects of insulin diminish,
potassium shifts back out of cells.

28. Therapies for elevated Potassium Levels:-
Calcium Gluconate IV. Generally used in advanced
cardiac toxicity (with evidence of hyperkalemic ECG
changes). Calcium raises the threshold for excitation,
resulting in dysrhythmias.
 Treatments that removes potassium from the body.
Sodium polystyrene sulfonate (Kayexalate) and
dialysis.

29. Therapies for elevated Potassium Levels:-
Sodium polystyrene sulfonate (Kayexalate). Cation-
exchange resin is administered by mouth or retention
enema. When resin is in the bowel, potassium is
exchanged for sodium. Therapy removes 1 mEq of
potassium per gram of drug. It is mixed in water with
sorbitol to produce osmotic diarrhea, allowing for
evacuation of potassium-rich stool from body.
 Dialysis for immediate remedy.

30. Conservative therapy IN AKI is all that is necessary until
kidney function improves. Controversy exists about the
timing of renal replacement therapy (RRT) in AKI.
Even though peritoneal dialysis (PD) is considered a viable
option for RRT, it is not frequently used. Intermittent
hemodialysis (HD) (at intervals of 4 hours either daily,
every other day, or 3 or 4 times per week) and continuous
renal replacement therapy (CRRT) have both been used
effectively.
CRRT is provided continuously over approximately 24
hours through cannulation of an artery and vein or
cannulation of two veins.

31. Nutritional Therapy:
– Maintain adequate caloric intake (30 to 35 kcal/kg
and 0.8 to 1 g of protein per Kg of body weight).
– Regulate potassium and sodium levels.
– Increase dietary fat intake
– Minimize fluid volume

32. Concept Map of AKI

33. The kidneys filter waste and excess water from your
blood as urine. Chronic kidney disease causes
your kidneys to lose this function over time. End-
stage kidney disease is the final stage of chronic
kidney disease. It means your kidneys no longer
function well enough to meet the needs of daily
life.
The kidneys of people with ESRD function below 10
percent of their normal ability, which may mean
they’re barely functioning or not functioning at
all.

34. CKD is irreversible and progressive reduction of
functioning of renal tissue.
Structural or functional abnormalities of the
kidneys for >3 months, as manifested by either:
1. Kidney damage, with or without decreased GFR, as
defined by
• pathologic abnormalities
• markers of kidney damage, including abnormalities
in the composition of the blood or urine or
abnormalities in imaging tests
2. GFR <60 ml/min/1.73 m2, with or without kidney damage

35. In India, it has been recently estimated that the age-
adjusted incidence rate of ESRD to be 229 per million
population (pmp), and >100,000 new patients enter
renal replacement programs annually.
In the US, the incidence is 338 new cases pmp.
Approximately 28% have a functioning
transplant, 66%recevice hemodialysis, and
5.7% are undergoing a form of peritoneal
dialysis.

36. Although chronic kidney disease sometimes results from
primary diseases of the kidneys themselves, the major
causes are diabetes and high blood pressure.
• Type 1 and type 2 diabetes mellitus cause a
condition called diabetic nephropathy.
• High blood pressure (hypertension), if not
controlled, can damage the kidneys over time.
• Glomerulonephritis
• Polycystic kidney disease is a hereditary cause of
CKD

37. • Use of some drugs over long time
• Clogging and hardening of the
arteries (atherosclerosis)
• Obstruction of the flow of urine by stones,
an enlarged prostate, strictures (narrowings), or
cancers may also cause kidney disease.
• Other causes of chronic kidney disease include HIV
infection, sickle cell disease, heroin abuse,
amyloidosis, kidney stones, chronic kidney infections,
and certain cancers.
• AKI

38. If one has any of the following conditions, they are at
higher-than-normal risk of developing chronic kidney
disease. One's kidney function may need to be
monitored regularly.
• Diabetes mellitus type 1 or type 2
• High blood pressure
• High cholesterol
• Heart disease
• Liver disease
• Amyloidosis
• Sickle cell disease

39. • Vascular diseases such as arteritis, vasculitis or
fibromuscular dysplasia
• Vesicoureteral reflux (a urinary tract problem in which
urine travels from the bladder the wrong way back
toward the kidney)
• Require regular use of anti-inflammatory medications
• A family history of kidney disease
• Being African-American, Hispanic, Native American or
Asian
• Being over 60 years old
• Obesity

40. • Traditionally, the classification of the type of
CKD has been focused on pathology and
etiology. The Kidney Disease Outcome Quality
Initiative (K/DOQI) classification system
focuses on GFR, but remains important to
diagnose the cause of CKD.

41. Sta
ge
Description Other Terms Used
GFR
(ml/min/
1.73m2)
1 Kidney damage with normal
GFR
At risk >90
2 Kidney damage with mild
decrease in GFR
Chronic renal
insufficiency (CRI)
60 - 89
3 Moderate decrease in GFR CRI, Chronic renal
failure (CRF)
30 - 59
4 Severe decrease in GFR CRF 15 - 29
5 Kidney Failure ESRD <15

43. With the deterioration and destruction of nephrons there
will be progressive loss of renal functions. As the GFR &
clearance is , Sr. Urea, nitrogen and Cr. .
To make this solutes filters out hypertrophy of nephrons
occurs. As a consequence the kidney lose their ability
to concentrate urine and a large volume of dilute urine
passes which may make fluid depletion. The tubules
gradually lose their ability to reabsorb electrolyte
result in lose of salt through urine leads to ployuria.
As the renal damage advances and no:of functional
nephrons declines, GFR decreases further and results
in uremia and death.

44. Patients with chronic kidney disease (CKD) stages 1-
3 (glomerular filtration rate [GFR] >30
mL/min/1.73 m²) are frequently asymptomatic.
When the glomerular filtration rate (GFR) slows to
below 30 mL/min, signs of uremia (high blood
level of protein by-products, such as urea) may
become noticeable. When the GFR falls below 15
mL/min most people become increasingly
symptomatic.

46. History and physical examination
Identification of reversible kidney disease
Blood test: BUN, Sr. Cr., electrolyte, lipid profile,
Hb and hematocrit
Urine analysis
USG
Renal scan
CT/MRI
Renal biopsy

48. COMPLICATIONS

49. Goal
To preserve existing kidney function
Reduce the risk of CV disease
Prevent complications
Provide for patient’s comfort

50. Correction of extracellular fluid volume overload or
deficit
Nutritional therapy
Erythropoietin therapy
Calcium supplementation, phosphate binders, or both
Antihypertensive therapy
ACE inhibitors or ARBs
Measures to treat hyperlipidemia
Measures to treat hyperkalemia
Adjustment of drug dosage to degree of renal function
RRT – Dialysis/Renal transplant

51. Drug Therapy
Hyperkalemia
Multiple strategies are used with dietary restriction
and drugs.
– IV glucose & insulin
– IV 10% calcium gluconate
– Sodium polystyrene sulfonate
– Dialysis may be required

52. Drug Therapy
Hypertension
• Target BP < 130/80 mm Hg
• Weight lose (if obese)
• Therapeutiic lifestyle changes
• DASH diet
• Administer antihypertensive drugs – ACE
inhibitors & ARBs

53. Drug Therapy
CKD-MBD
• Limiting dietary phosphorus
• Administer phosphate binders – calcium
acetate, calcium carbonate
• Supplemental calcium and vitamin D
• If hyperparathyroid disease persist – subtotal or
total parathyroidectomy

54. Drug Therapy
Anemia
• Exogenous erythropoietin (EPO) – epoetin alfa,
darbepoetin alfa. (in low doses)
• Iron supplement if plasma ferritin concentrations falls
• Folic acid supplement
• Avoid blood transfusion as it can cause iron overload
Dyslipidemia – best managed with statins

55. Nutritional Therapy