07/03/23

ARF, CRF
Dr. Salman Ansari
MBBS
● ARF
● CRF
● Charts
ACUTE RENAL FAILURE

New name: AKI

ARF

● Definition
● Causes
● Pathogenesis
● Morphology
● Stages
● Clinical features
● Diagnosis, treatment
Acute Renal Failure(ARF)

● Definition: rapid reduction of renal function, with severe

oliguria
● Now known as AKI(acute kidney injury)
● ATI is the most common cause of acute kidney injury(acute renal
failure)
● ATI →AKI/ARF
● Commonly seen in hospital setting
● Very common in ICU patients
KDIGO criteria

According to KDIGO(Kidney Disease: Improving Global Outcomes), AKI is

the presence of any of the following:

1. Increase in serum creatinine by 0.3 mg/dL or more (26.5

micromoles/L or more) within 48 hours
2. Increase in serum creatinine to 1.5 times or more baseline within the
prior seven days
3. Urine volume less than 0.5 mL/kg/h for at least 6 hours
Causes of AKI

Divided into 3 categories

Post-renal
Pre-renal Renal (5%)
(60%) (35%)
1. Pre-renal

Any cause that reduces blood flow to kidney

● Fluid loss: due to blood loss, burns, diarrhoea, vomiting
● Hypotension: shock, pulmonary embolism
● Medications which cause renal vasoconstriction: NSAIDs, ACEI,
ARBs, iodinated contrast, metformin
2. Renal

Any condition which affects the tubules or glomeruli of kidney

● Acute tubular necrosis(ATN)
● Acute glomerulonephritis(AGN)
● Medications which cause acute interstitial nephritis(AIN): clavulanic
acid, penicillins, NSAIDs
3. Post-renal

Any obstruction to urine flow

● Renal stones
● Blocked catheter
● tumours
● BPH(benign prostatic hyperplasia) in older men
 Pre-renal Renal Post-renal

Fluid loss: bleeding, Acute tubular Renal calculi

burns diarrhoea, vomiting necrosis(ATN)

Hypotension: shock Acute Blocked catheter

glomerulonephritis(AGN)

Drugs: Acute interstitial BPH

● NSAIDs nephritis(AIN) due to Tumours
● Diuretics drugs like:
● Contrast dye ● NSAIDs
● ACEI/ARB ● Penicillins
● Metformin ● Clavulanic acid
Pathogenesis of AKI
Injury to tubular epithelial cells, due to ischemia/toxins
↓
Leads to back-leakage of fluid from lumen into interstitium
↓
Damaged tubular epithelial cells detach and form casts, which blocks the lumen
↓
Luminal obstruction leads to: (1)increased tubular pressure, (2) decreased GFR
and (3) decreased urine flow
↓
Ischemia also causes vasoconstriction which reduces GFR and oxygen supply
to tubules
↓
Acute tubular injury → Acute kidney injury
Morphology
Ischemic kidney injury

Gross
Both kidneys are swollen with a pale cortex and congested medulla
Microscopy
● Glomeruli: normal
● Tubules: focal and multiple areas of damage, most prominently in
proximal tubules and ascending limb of loop of Henle
● Interstitium: edema, leukocytes
● Blood vessels: normal
Toxic kidney injury
Toxic kidney injury
Microscopy:
● Proximal convoluted tubule(PCT) is affected most commonly
● More necrosis is seen as compared to ischemic ATN
Clinical course
3 stages:
1. Initiation phase ● Mild ↓urine output, ↑ in BUN
2. Maintenance ● ↓↓ in urine output(oliguria), salt and
phase water overload, rising BUN,
●3. Steady
Recovery ↑ inphase
urine volume hyperkalemia, metabolic acidosis and
● Loss of large amounts of other features of uremia
water, Na and K in
urine(leads of
hypokalemia)
Clinical course
3 stages:
1. Initiation phase ● Mild ↓urine output, ↑ in BUN
2. Maintenance ● ↓↓ in urine output(oliguria), salt and
phase water overload, rising BUN,
●3. Steady
Recovery ↑ inphase
urine volume hyperkalemia, metabolic acidosis and
● Loss of large amounts of other features of uremia
water, Na and K in
urine(leads of
hypokalemia)
Clinical features

● Decreased or no urine output

● Edema
● Nausea
● Weight gain
● Shortness of breath
● Hypertension
● Confusion
Diagnosis

● ↓ urine volume
● RFT: S. urea, S.creat ↑
● hyperkalemia
● eGFR: 🙅 not useful in AKI 🙅
Treatment

● AKI is often reversible

● Treatment depends upon the cause(pre/renal/post)
● Maintain BP and urine output
● If hypovolemic: give IV fluids
● I/O monitoring
● Hyperkalemia: treated by dietary restriction or medications(insulin)
● Stop any nephrotoxic drugs (Mnemonic:“stop the DAMN” drugs)
● If obstruction suspected: do USG abdomen and pelvis D - Diuretics
● Dialysis A - ACEI/ARB
M - Metformin
N - NSAIDs
CHRONIC RENAL FAILURE
CRF

● Definition
● Causes
● Pathogenesis
● Stages of CRF
● Clinical features
● Diagnosis, treatment
Chronic renal failure
Definition: gradual and irreversible decline in renal function due to
slow destruction of renal tissue
● Kidneys will be shrunken
● GFR less than 50% or <60 ml/min, for 3 months or more
Etiology
1, Diseases affecting glomerulus:
● Chronic glomerulonephritis
● diabetic nephropathy
2. Diseases affecting tubules and interstitium:
● Vascular: long-standing hypertension
● Infectious: chronic pyelonephritis
● Toxic: long-term use of nephrotoxic
drugs(aspirin, paracetamol), lead
● Obstruction: tumours, kidney stones
Pathogenesis

1. Damage to glomerulus leads to changes in filtration, and

development of nephrotic syndrome(proteinuria, hypoalbuminemia
and oedema)

2. Damage to tubules leads to changes in reabsorption and secretion

of important substances, leading to excretion in large amounts of
dilute urine
Stages of CRF

5 stages, depending upon the GFR

1. Normal: GFR: 50-100%
2. Decreased renal reserve: GFR is <50%
3. Renal insufficiency: GFR: <25%
4. Renal failure: GFR: <10%
5. End-stage kidney disease: GFR: <5%
Clinical features

- Renal symptoms + extra-renal symptoms

Renal symptoms:
● Metabolic acidosis: Kussmaul breathing(rapid, deep breathing)
● Hyperkalemia: weakness, nausea, cardiac arrhythmia, diarrhoea
● Sodium and water imbalance: congestive heart failure
● Hyperuricemia: uric acid crystals in joints and soft tissues - “gout”
● Azotaemia: high serum urea, creatinine
Non-renal symptoms:
● Anemia(due to decreased production of erythropoietin)
● Yellowing of skin
● Congestive heart failure
● Pulmonary oedema
● Renal osteodystrophy
Diagnosis of CKD

● CBC: anemia
● Hyperkalemia
● RFT(renal function tests): increased serum urea, serum creatinine
● eGFR(estimated GFR): reduced to <50% or <60 ml/min
● USG Abdomen and Pelvis: shrunken kidneys
● Biopsy may be needed
Treatment

● No cure - treatment can only slow the disease

● Lifestyle changes, “renal diet”: low salt, protein and phosphorous
● Maintain BP
● Control blood sugar in diabetics
● Treat uremia by:
● Dialysis: 2 types - hemodialysis and peritoneal dialysis
● renal transplant

Mnemonic: “LMCT” - Let Me Cure This

CHART - Renal system - 1
A 56 year old women is diagnosed with diabetes since 25 years. On examination, she has a
blood pressure of 168/110 mmHg. Patient appears pale. No other abnormalities identified.

Her investigations show:

Urinalysis Blood

pH: 7.0 S. urea nitrogen: 71 mg/dl

Spec. grav: 1.010 Creatinine: 4.7 mg/dl

Proteinuria: 2+ Hemoglobin: 9 mg/dl

Urine glucose: Positive
Abdominal USG shows bilateral symmetrically small kidneys

Questions: 1) What is the most likely diagnosis? 2) Why do you say so?

3) What is the other common condition that can progress to this condition?

4) Why is the patient anemic?

Questions: 1) What is the most likely diagnosis? 2) Why do you say so?

3) What is the other common condition that can progress to this condition?

4) Why is the patient anemic?

Answers:
1) Chronic renal failure
2) Deranged S. urea and creatinine in the presence of shrunken kidneys
3) Long-standing hypertension
4) In CRF, the kidneys are not able to produce enough erythropoietin(EPO), thus
there is decreased synthesis of RBCs, leading to anemia.
CHART - Renal system - 2
A 54 year old male with a history of coronary artery disease came with complaints
of increasing tiredness since last month. He also said that his abdomen was
growing larger in size and he had gained 15 kg over the past month. During the
past week he has had breathlessness and his feet have swollen. Cardiac echo
shows ejection fraction of 30%.
On physical examination, the patient is in moderate respiratory distress. BP is
140/80mmHg, pulse 95/min and RR 28/min. Body weight: 91 kg. Abdomen is
enlarged with a positive fluid wave. Lower extremities showed pitting oedema.
Lab data

May July 1 July 2 July 3 Normal

Sodium 130 133 134 133 136-146 mmol/L

Potassium 4.9 5.7 5.8 6.0 3.5-5.0 mmol/L

Chloride 100 90 91 93 102-109 mmol/L

BUN 20 87 94 101 7-20 mg/dl

Creatinine 0.9 3.0 3.5 3.7 0.6-1.2 mg/dl

Renal ultrasound: right kidney 10 x 5.5, left kidney 10.5 x 6.0. Both kidneys
demonstrate normal echogenicity and are without masses or cysts. There is no
hydronephrosis.
Questions:
1) Is the type of kidney injury acute or chronic? Why?
2) What is the cause of kidney injury in this case?
Answers:
A1) Acute kidney injury
Reasons:
- Symptoms are of short duration(1 month)
- Sudden rise in urea and creatinine levels in a short span of time
- Ultrasound shows kidneys of normal echogenicity

A2) AKI is because of his heart failure.

The ejection fraction is low(30%), which means the heart is not able to pump blood
with enough pressure to maintain the GFR. Therefore the kidneys are not able to
clear urea and creatinine from the body adequately, leading to rise of blood levels of
the same.
References: For PPT, scan:
● Ramadas Nayak - Textbook of Pathology for Allied Health
Sciences
● StatPearls - Acute kidney injury
● StatPearls - Chronic renal failure

Questions:

salman.s.ansari92@gmail.com

For notes, scan: