Renal

Failure
By Ms. Seemab Ashraf
 Renal Failure
Renal failure is a condition where one or both the kidneys fail to
perform their normal function of filtering waste products from the
blood and regulating fluid and electrolyte balance. This can lead to the
buildup of harmful waste products in the blood, electrolyte
imbalances, and fluid overload.
 Types
Acute Renal Failure or
Acute Kidney Injury

Chronic Renal Failure or

Chronic Kidney Disease
 Acute Kidney Injury
Acute Renal Failure (ARF), also known as Acute Kidney Injury (AKI) is a
sudden, rapid and potentially reversible decline in kidney function that occurs
over hours to days which resulting in retention of nitrogenous waste products
in body fluids.
 Types of AKI
Three types based on the location and the cause of the injury:

❑ Pre-renal AKI: Decrease in blood flow to the kidneys, leading to decreased

urine output and kidney function. Causes include severe dehydration, blood loss,
heart failure, trauma, contrast media, use of NSAIDs, anti-hypertensive drugs,
and cyclosporine.

❑ Intra-renal AKI: Damage to the kidney tissue itself, such as from infections,
medication toxicity, or autoimmune diseases. Diseases include acute tubular
necrosis, interstitial nephritis, glomerulonephritis, vasculitis and rhabdomyolysis.

❑ Post-renal AKI: Obstruction to the flow of urine from the kidneys, leading to
an accumulation of urine and increased pressure within the kidneys. Causes
include kidney stones, tumors, and enlarged prostate gland.
4 Phases of AKI
4 Phases of AKI
 Risk Factors of AKI
❑ Advanced age
❑ Chronic Kidney Disease (CKD)
❑ Diabetes
❑ Heart disease
❑ Liver disease
❑ Medicines
❑ Dehydration
❑ Infections
❑ Surgery involving kidney or urinary tract
Symptoms of AKI
Complications of AKI
 Diagnosis of AKI
Diagnosis of AKI typically involves a combination of clinical assessment, laboratory
tests, and imaging studies.

❑ Clinical Assessment:
❑ Patient's symptoms
❑ Medical history
❑ Medication history and
❑ Physical exam
 Diagnosis of AKI
❑ Laboratory tests:
❑ Serum creatinine (Scr): Normal range is approx. 0.6-1.3 mg/dL for adult men and
0.5-1.2 mg/dL for adult women.
In AKI, Scr levels typically rise rapidly and can be used to estimate the severity.
❑ BUN: Normal range is approx. 7-20 mg/dL.
Elevated BUN levels indicate decreased kidney function
❑ Urine Output: Normal range is 0.5-1.5 mL/kg/hour in adults.
Decreased urine output can be an early sign of AKI.
❑ Urinalysis: Helps to identify the presence of RBCs, WBCs, protein, or other
abnormalities in the urine.
❑ Electrolyte levels: Electrolyte levels like sodium, potassium, and calcium, can be
affected by AKI and may require monitoring and treatment to prevent
complications.
 Diagnosis of AKI
❑ Imaging studies:
Ultrasound, CT scan, or MRI may be used to diagnose and evaluate the
severity of AKI and to identify any underlying structural or functional
abnormalities that may be contributing to the condition.
 KDIGO Criteria
❑ The Kidney Disease Improving Global Outcomes (KDIGO) criteria are widely used
to diagnose and classify AKI.
❑ AKI is defined as an increase in serum creatinine by ≥ 0.3 mg/dL within 48 hours,
or an increase in serum creatinine to ≥1.5 times baseline within the prior 7 days,
or urine output <0.5 mL/kg/h for 6 hours.
❑ The KDIGO criteria also divide AKI into three stages:
 Treatment of AKI
❑ Treatment of AKI is mainly supportive.
❑ Goal is to assure adequate renal perfusion by achieving and maintaining
hemodynamic stability and avoiding hypovolemia.
❑ If fluid resuscitation is required because of hypovolemia, isotonic solutions (e.g.,
normal saline) are preferred. A reasonable goal is a mean arterial pressure >65
mm Hg, which may require the use of vasopressors in patients with persistent
hypotension.
❑ Correction of electrolyte abnormalities is important.
❑ Hyperkalemia (IV Regular insulin with 50% dextrose solution can shift
potassium out of circulation and into the cells, calcium gluconate (10 mL of
10% solution infused IV over five minutes)
❑ Correction of metabolic acidosis with bicarbonate administration
❑ Correction of hyponatremia (administration of hypertonic saline in severe
cases)
 Treatment of AKI
❑ Correction of fluid overload with loop diuretics like furosemide and bumetanide.
(furosemide initial dose is 20-40 mg IV, with subsequent doses titrated based
on the patient's response)
❑ Correction of hematologic abnormalities
❑ All nephrotoxic agents (e.g. Radiocontrast agents, antibiotics with nephrotoxic
potential, heavy metal preparations, cancer chemotherapeutic agents, NSAIDs)
should be avoided or used with extreme caution.
❑ Doses of all medications cleared by renal excretion should be adjusted.
 Dietary Modification
Dietary changes are an important facet of AKI treatment and which depends on the
stage and severity of the condition.
❑ Control fluid intake
❑ Restriction of potassium and phosphorus in the diet
❑ Limit the intake of protein
 Dialysis
❑ Indications for dialysis in patients with AKI are as follows:
❑ Diuretic resistant fluid overload or refractory pulmonary edema.
❑ Hyperkalemia with ECG changes or refractory to medical therapy (>6.5 mmol/L)
❑ Metabolic acidosis refractory to medical therapy (pH less than 7.2)
❑ Severe azotemia (BUN >100mg/dL)
❑ Sudden increase in Scr by > 0.5 mg/dL/hr or > 4.5 mg/dL within 48 hours
❑ Uremic symptoms like pericarditis, encephalopathy, or bleeding due to uremic
platelet dysfunction.

❑ Peritoneal dialysis is not frequently used in patients with AKI.

 Chronic Kidney Disease
❑ CKD is defined as the presence of kidney damage or an estimated GFR less than
60 ml/min/1.73m2, persisting for 3 months or more irrespective of the cause.
❑ It is a state of progressive loss of kidney function ultimately resulting in the
need for renal replacement therapy (dialysis or transplantation).
❑ According to WHO, CKD affects approximately 10% of the global population, and
it is estimated that around 1 in 9 adults worldwide have some form of CKD.
❑ A study in 2020 reported a prevalence of 18.3% CKD among adults in Pakistan.
❑ Men are more likely to develop CKD than women.
Risk Factors
Chronic Diseases

Family history of kidney disease

Older Age

Obesity

Smoking

Cardiovascular disease

Chronic urinary tract infections

 Causes of CKD
❑ Diabetes
❑ High blood pressure
❑ Glomerulonephritis
❑ Interstitial Nephritis
❑ Polycystic kidney disease
❑ Kidney infections and urinary tract obstructions
❑ Prolonged use of certain medications
❑ Other conditions like lupus, multiple myeloma, HIV/AIDS, and amyloidosis.
 Pathogenesis of CKD
❑ Multiple factors cause progressive damage and dysfunction of the kidneys
❑ Ongoing inflammation and oxidative stress damage the delicate structures of the
kidney, including the glomeruli, tubules, and interstitium. This lead to fibrosis
and scarring, which in turn can impair kidney function and further perpetuate
inflammation and oxidative stress.
❑ Another important factor is the presence of chronic diseases which can damage
the blood vessels that supply the kidneys and disrupt the normal filtration
process resulting in accumulation of waste products and fluid in the body, as well
as imbalances in electrolytes and other important substances.
 Symptoms of CKD
In the early stages, CKD may not cause any noticeable symptoms. As the disease
progresses, however, symptoms may develop, including:
❑ Swelling
❑ Shortness of breath
❑ Changes in urination (frequency or amount of urine)
❑ Nausea and vomiting
❑ Fatigue and weakness
❑ Difficulty sleeping
❑ Itchy skin
❑ Muscle cramps
❑ Loss of appetite
 Complications of CKD
CKD can lead to a range of complications, both due to the underlying disease itself
and to the treatments used to manage it. Some of the common complications of CKD
include:
❑ Cardiovascular disease
❑ Fluid overload
❑ Anemia
❑ Malnutrition
❑ CNS problems
❑ Bone disease due to imbalances in calcium and phosphorus levels in the body
❑ End-Stage Kidney Disease
❑ Decreased quality of life (physical and emotional symptoms, social isolation, and
financial stress related to the cost of treatment)
Stages of CKD (KDIGO Criteria)
 Stages of CKD (KDIGO Criteria)
❑ Stage 1: There are often no symptoms in this stage, and kidney damage may be
detected only by laboratory tests.
❑ Stage 2: There may still be no symptoms in this stage, but there may be an increased
risk of complications.
❑ Stage 3: Symptoms such as fatigue, fluid retention, and changes in urination may
begin to appear.
❑ Stage 4: Kidney function is severely reduced. Symptoms such as nausea, vomiting, and
muscle cramps may become more severe, and there is an increased risk of
complications.
❑ Stage 5: This is also known as End-Stage Renal Disease (ESRD). In this stage, kidney
function is very severely reduced or has completely failed. Dialysis or a kidney
transplant is typically required to manage the condition.
 Diagnosis of CKD
The diagnosis of CKD typically involves a combination of medical history, physical
examination, laboratory tests, and imaging studies.
Common diagnostic tests used in CKD are:
❑ Blood tests: Like Scr and Blood Urea Nitrogen (BUN)
❑ Urine tests: Urinalysis and urine albumin-to-creatinine ratio (UACR)
❑ Imaging studies: Ultrasound, CT scan, and MRI to evaluate the size and
structure of the kidneys and detect any abnormalities.
❑ Kidney biopsy: Necessary in some cases to evaluate the severity and type of
kidney disease.
Based on the results, determine the stage of CKD and develop a treatment plan to
slow the progression of the disease and manage symptoms.
 Treatment of CKD
❑ Early diagnosis and treatment of the underlying cause is imperative in patients
with CKD.

❑ The medical care of patients with CKD should focus on the following:
❑ Delaying or halting the progression of CKD
❑ Diagnosing and treating the pathologic manifestations of CKD
❑ Planning for Renal Replacement Therapy
 Delaying Progression of CKD
❑ Treatment of the underlying condition if possible
❑ Aggressive blood pressure control to target values per current guidelines
❑ Treatment of hyperlipidemia to target levels
❑ Aggressive glycemic control (target HbA1C < 7%)
❑ Use of sodium–glucose cotransporter 2 (SGLT2) inhibitors like dapagliflozin
❑ Avoidance of nephrotoxins, including IV radiocontrast media, NSAIDs, and
aminoglycosides
❑ Use of ACE inhibitors or ARBs in patients with proteinuria
 Treating Pathologic Manifestations of CKD
❑ Anemia: ESA like epoetin alfa or darbepoetin alfa
❑ Hyperphosphatemia: Treat with dietary phosphate binders and dietary phosphate
restriction
❑ Hypocalcemia: Treat with calcium supplements with or without calcitriol (Rocaltrol®).
❑ Hyperparathyroidism: Treat with calcitriol, vitamin D analogues, or calcimimetics
❑ Volume overload: Treat with loop diuretics
❑ Metabolic acidosis: Treat with sodium bicarbonate
❑ Uremic manifestations: Treat with long-term RRT (hemodialysis, peritoneal dialysis,
or kidney transplantation)
❑ Cardiovascular complications: Treat as appropriate (statin therapy)
 Renal Replacement Therapy
❑ Choice of RRT depends on patient's medical condition, lifestyle, preferences, and
resources.

Hemodialysis

Peritoneal Dialysis

Kidney Transplantation
 Hemodialysis
❑ During the treatment, blood is removed from the body through a surgically
implanted access point, passed through a dialyzer, which is a machine that
filters out excess fluid and waste products, and then returned to the body.
This is usually done at a dialysis center or hospital, typically three times a
week for four hours per session.
 Peritoneal Dialysis
❑ In peritoneal dialysis, the patient's own peritoneum (a membrane lining the abdominal
cavity) is used as a filter. A dialysate fluid is a mixture of sterile electrolyte solutions
which is introduced into the peritoneal cavity through a catheter, where it remains for
several hours before being drained out. Excess waste and fluid pass from the blood
vessels into the dialysate fluid. The fluid is then drained out and discarded.
 Kidney Transplant
❑ Kidney transplantation is the most effective form of renal replacement therapy,
offering the best long-term survival and quality of life.
❑ In a kidney transplant, a healthy kidney is surgically placed into the patient's body,
usually in the lower abdomen near the pelvis.
❑ The transplanted kidney takes over the function of the failed kidneys, allowing the
patient to return to a more normal life. Kidney transplants can come from living or
deceased donors.
 Non-Pharmacological Management
Weight loss

Smoking cessation

Limiting protein, sodium, potassium, and phosphorus intake

Regular exercise for at least 30 minutes 5 times per week

Stress Management