Renal failure by dr hari sharan aryal

Renal Failure
Presenter:
Dr Hari Sharan Aryal
MD (Ayu), IOM, TU
Department of Kayachikitsa
TUATH, Kirtipur

Contents:
Functional Anatomy and
Physiology of Kidney
Pathophysiology
Types
Causes
Sign and Symptoms
Differential Diagnosis
Investigations and Findings
Treatment
Complications if not treated
Reference
WorldKidneyDay12thMarch.
Renal Failure; Dr Hari Sharan Aryal; 2076.11.29 2

FunctionalAnatomy
&
Physiology:

Types :
Acute Renal Failure
(ARF) OR
Acute Kidney Injury
(AKI)
Chronic Renal Failure
(CRF) OR
Chronic Kidney Disease
(CKD)
Renal Failure

AKI Background:
Acute kidney injury (AKI), previously referred to as acute renal Failure
It describes the situation where there is a sudden and often reversible
loss of renal function Which develops over days or weeks accompanied by
a reduction in urine volume.
It is important to recognize that AKI is a clinical diagnosis and not a
structural one.

AKI Background: …
Using consensus criteria, an estimated 20% of hospitalized
patients develop AKI, and nearly 60% of intensive care unit
patients incur AKI
Greater than 40% of hospital-associated AKI is iatrogenic
Most common cause of AKI in hospitalized patients is intrinsic
kidney failure caused by acute tubular necrosis (ATN) and prerenal
disease

AKI Causes :
• Prerenal: inadequate renal perfusion caused by hypovolemia,
congestive heart failure (impaired cardiac output), cirrhosis (fluid
third-spacing), sepsis (vasodilation), abdominal compartment
syndrome, or other. Sixty percent of community-acquired cases of
AKI are from prerenal conditions.
• Postrenal: bladder outlet obstruction (prostatic
enlargement, urethral fibrosis), ureteral obstruction (stones, bladder
masses, retroperitoneal fibrosis, ureteral fibrosis), or renal vein
occlusion. With two functioning kidneys, bilateral obstruction is
usually required to cause significant AKI. Postrenal causes of AKI
account for 5% to 15% of community acquired AKI.
• Intrinsic renal: ATN, glomerulonephritis, AIN. Common causes of
ATN include ischemia (e.g., hypotension or shock, post cardiac bypass
or aorta surgery), rhabdomyolysis, sepsis, drug toxicity (e.g.,
aminoglycosides, amphotericin, cisplatin), and iodinated radiocontrast
nephropathy. Contrast-induced nephropathy is the third-most common
cause of new-onset AKI in hospitalized patients. AIN can develop after
exposure to a variety of medications, most commonly nonsteroidal
anti-inflammatory drugs, antibiotics, and proton pump inhibitors
Poisonous Mushroom ,Heavy
Metals and Semicarpus Causes
ATN.

AKI Types :
Prerenal ARF
Intrinsic renal ARF
Postrenal ARF.

AKI Prerenal Causes :
−− Hypovolemia
–– Hemorrhage
–– Burn
–– Dehydration
–– Gastrointestinal (GI) fluid loss
–– Renal fluid loss
–– Sequestration (acute pancreatitis).
−− Low cardiac output
–– Acute myocardial infarction (AMI)
–– Arrhythmia
–– Pulmonary embolism.
−− Impaired renal autoregulation
–– Systemic vasodilation caused by:
»» Anesthesia
»» Anaphylaxis
»» Sepsis
»» ACE–I.
–– Renal vasoconstriction by:
»» Hypocalcemia
»» Epinephrine, norepinephrine
»» Amphotericin–B
»» Cyclosporine
»» Hepatorenal syndrome
»» NSAID
»» ACE–I.

AKI Renal Causes :
Causes of intrinsic renal ARF
−− Renal artery obstruction by
atherosclerotic, plaque,
thrombosis, embolism, vasculitis.
−− Renal vein obstruction by
thrombosis/compression.
−− Disease of the glomeruli and renal
micro- vasculature:
–– Glomerulonephritis and vasculitis.
–– Secondary diseases
—Hemolytic uremic syndrome (HUS),
(DIC), Systemic lupus erythematosus
Progressive systemic sclerosis (PSS),
toxemia of pregnancy and malignant HTN.
−− Causes of acute tubular necrosis
(ATN)
–– Ischemic causes of ATN—Causes are
same as prerenal ARF.
Due to vasoconstriction of efferent arteriole
in severe hypovolemia leads to severe
decrease in blood supply to tubular cells.

AKI Renal Causes : …
Nephrotoxic substance causing ATN
»» Exogenous—Radiocontrast dye,
aminoglycoside,
paracetamol, solvent like ethylene
glycol,
cyclosporine and cisplatin.
»» Endogenous—Myoglobin,
hemoglobin, uric
acid, oxalate and myeloma protein.
−− Interstitial nephritis—Responsible
for ATN
–– Allergic causes:
»» β-lactam and sulfonamide
»» Trimethoprim and rifampicin
»» NSAID and captopril.
–– Infections:
»» Pyelonephritis
»» Leptospirosis
»» CMV
»» Candida.
–– Idiopathic
–– Infiltration:
»» Lymphoma
»» Leukemia
»» Sarcoidosis.
−− Renal allograft rejection.

AKI Postrenal Causes :
Postrenal:
Bladder outlet obstruction (prostatic enlargement, urethral fibrosis)
Ureteral obstruction (stones, bladder masses, retroperitoneal
fibrosis, ureteral fibrosis), or renal vein occlusion.
With two functioning kidneys, bilateral obstruction is usually required to
cause significant AKI.
Postrenal causes of AKI account for 5% to 15% of community acquired AKI.

AKI Stages: …
The acronym RIFLE is used to define the spectrum of progressive Kiney Injury in
AKI.
Risk: 1.5 fold increase in serum creatinine or GFR decrease by 25% for 6 hours.
Injury: 2 fold increase in serum creatinine or GFR decrease by 50% for 12 hours.
Failure: 3 fold increase in serum creatinine or GFR decrease by 75% for 24 hours
or no urine output for 12 hours.
Loss: Complete loss of Kidney Function ( eg. Need for Renal Replacement
Therapy) for more than 4 weeks.
End-Stage Kidney Disease: Complete loss of Kidney Function ( eg. Need for Renal
Replacement Therapy ) for more than 3 months.

AKI Sign & Symptoms:
Symptoms
Oliguria (urine output < 500 mL/day). But oliguria may not be always present.
Increase thirst
Orthostatic dizziness and hypotension
Tachycardia
Decreased skin turgor
Dry mucous membrane
Reduced sweating in axilla
Reduced jugular venous pressure.

AKI Sign & Symptoms: …
Signs
Flank pain is due to:
− Renal artery/vein occlusion.
− AGN produce pain by distending
the renal capsule.
Pyelonephritis and obstructive
uropathy can produce -- pain.
Digital ischemia—Indicates
atheroembolism as a cause for ARF.
ARF with oliguria, hypertension,
edema and active urinary sediment
indicate AGN or vasculitis.
Very high BP in malignant HTN can
cause ARF which is associated with
LVH/LVF/papilledema/neurologic
dysfunction.
Fever, arthralgia and pruritus following
some drugs may cause allergic
interstitial nephritis.

AKI Sign & Symptoms: …
SPECIAL POINTS OF POSTRENAL ARF
Suprapubic and flank pain is a feature
of distention of bladder or renal pelvis
and capsule.
Colicky pain radiating to groin suggests
ureteric colic due to obstruction.
Prostatic disease is suggested by
nocturia, frequency, hesitancy, difficulty
in initiation, narrow stream and
confirmed by rectal examination of
prostate or USG of kidney ureter
bladder prostate (KUBP).
Neurogenic bladder is caused by
anticholinergic drugs, autonomic
dysfunction and paraplegia due to
spinal cord injury

AKI Differential Diagnosis :
Causes of AKI Some Clinical Features Typical Urinalysis
Result
Confirmatory Tests
Diseases
Involving Large
Renal Vessels:
Renal artery
thrombosis
History of atrial fibrillation or recent
myocardial infarction, nausea, vomiting,
flank or abdominal pain
Mild proteinuria
Occasionally RBCs
Elevated LDH level
with normal
transaminase
levels, renal
arteriogram
Atheroembolism Usually age > 50 yr, recent manipulation
of aorta, retinal plaques, subcutaneous
nodules, palpable purpura, livedo
reticularis
Often normal
Eosinophiluria
Rarely casts
Eosinophilia,
hypocomplementem
ia, skin
biopsy, renal biopsy
Renal vein
thrombosis
Evidence of nephrotic syndrome or
pulmonary
embolism, flank pain
Proteinuria,
hematuria
Inferior
venacavogram,
Doppler flow
studies, MRV*

AKI Differential Diagnosis : …
Causes of AKI Some Clinical Features Typical
Urinalysis
Result
Confirmatory
Tests
Prerenal azotemia Evidence of true volume depletion
(thirst, postural or absolute
hypotension and tachycardia, low
jugular venous pressure, dry mucous
membranes and axillae, weight loss,
fluid output greater than input) or
decreased effective circulatory
volume (e.g., heart failure, liver failure),
treatment with NSAID, diuretic, or ACE
inhibitor/ARB
Hyaline casts
SG > 1.018
Occasionally
requires invasive
hemodynamic
monitoring; rapid
resolution of
AKI with
restoration of renal
perfusion

Causes of AKI Some Clinical Features Typical Urinalysis
Result
Confirmatory Tests
Diseases of
Small Renal
Vessels and
Glomeruli:
Glomerulonephri
tis or vasculitis
Compatible clinical history
(e.g., recent
infection), sinusitis, lung
hemorrhage, rash or skin
ulcers, arthralgia's,
hypertension, edema
RBC or granular
casts, RBCs, white
blood cells,
proteinuria
Low complement levels; positive
antineutrophil cytoplasmic antibodies,
anti–glomerular basement membrane
antibodies, anti–streptolysin O
antibodies, anti-DNase, cryoglobulins;
renal biopsy
HUS/TTP Compatible clinical history
(e.g., recent
gastrointestinal infection,
cyclosporine, anovulants),
pallor, ecchymoses,
neurologic Findings
May be normal,
RBCs, mild
proteinuria,
rarely RBC or
granular casts
Anemia, thrombocytopenia,
schistocytes
on peripheral blood smear, low
haptoglobin level, increased LDH,
renal biopsy
Malignant
hypertension
Severe hypertension with
headaches, cardiac failure,
retinopathy, neurologic
dysfunction, papilledema
May be normal,
RBCs, mild
proteinuria,
rarely RBC casts
LVH by echocardiography or ECG,
resolution of AKI with BP control

Causes of AKI Some Clinical Features Typical
Urinalysis Result
Confirmatory Tests
Ischemic or
Nephrotoxic Acute
Tubular Necrosis:
Ischemia
Recent hemorrhage, hypotension,
surgery often in combination with
vasoactive medication (e.g., ACE
inhibitor, NSAID)
Muddy-brown
granular or tubular
epithelial cell casts
SG ≈ 1.010
Clinical assessment and urinalysis
usually inform diagnosis
Exogenous toxin Recent contrast medium–
enhanced procedure; nephrotoxic
medications; certain
chemotherapeutic agents often
with coexistent volume depletion,
sepsis, or chronic kidney disease
Muddy-brown
granular or tubular
epithelial cell casts
SG ≈ 1.010
Clinical assessment and urinalysis
usually inform diagnosis

Causes of
AKI
Some Clinical
Features
Typical Urinalysis Result Confirmatory Tests
Endogeno
us toxin
History suggestive of
rhabdomyolysis
(coma, seizures,
drug abuse, trauma)
hemolysis (recent
blood transfusion)
tumor lysis (recent
chemotherapy),
myeloma (bone
pain), or ethylene
glycol ingestion
Urine supernatant tests
positive for heme in
absence of RBCs
Urine supernatant pink
and tests positive for
heme in absence of RBCs
Urate crystals, dipstick-
negative proteinuria,
oxalate crystals,
Respectively
Hyperkalemia, hyperphosphatemia,
hypocalcemia, increased CK,
Myoglobin
Hyperkalemia, hyperphosphatemia,
hypocalcemia, hyperuricemia, and
free circulating hemoglobin
Hyperuricemia, hyperkalemia,
hyperphosphatemia (for tumor
lysis); circulating or urinary
monoclonal protein (for myeloma);
toxicology screen, acidosis, osmolal
gap (for ethylene glycol)

Causes of AKI Some Clinical
Features
Typical Urinalysis Result Confirmatory Tests
Diseases of
the
Tubulointerst
itium:
Allergic
interstitial
nephritis
Recent ingestion
of drug and fever,
rash, loin pain, or
arthralgia's
White blood cell casts, white
blood cells (frequently
eosinophiluria), RBCs, rarely
RBC casts, proteinuria
(occasionally nephritic)
Systemic eosinophilia, renal biopsy
Acute bilateral
pyelonephritis
Fever, flank pain
and tenderness,
toxic State
Leukocytes, occasionally
white blood cell casts, RBCs,
bacteria
Urine and blood cultures
Postrenal AKI Abdominal and
flank pain,
palpable bladder
Frequently normal,
hematuria if
stones, prostatic
hypertrophy
Plain abdominal radiography, renal
ultrasonography, post void residual
bladder volume, computed
tomography, retrograde or antegradeRenal Failure; Dr Hari Sharan Aryal; 2076.11.29 24

AKI Investigations : …
LABORATORY TESTS
• Elevated serum creatinine: rate of rise is
approximately 0.5 to 2 mg/dl/day in
complete kidney failure.
• Elevated blood urea nitrogen (BUN): BUN
to- creatinine ratio is commonly >20:1 in
prerenal azotemia, Postrenal azotemia, and
acute glomerulonephritis.
• BUN-to-creatinine ratio is <20:1 in acute
interstitial nephritis and ATN.
• Hyperkalemia, hyperphosphatemia, and
metabolic acidosis are common.
• Hypocalcemia and hyponatremia or
hypernatremia may occur, depending on
underlying etiology.
• Complete blood count may reveal anemia
from decreased erythropoietin production.
• Urinalysis is the initial step of diagnostic
evaluation. Prerenal and Postrenal AKI are
typically characterized by a normal
urinalysis.

AKI Investigations : ...
IMAGING STUDIES
• ECG for arrhythmia detection, especially
in hyperkalemia: peaked T waves in
precordial leads, widening QRS interval,
and/or bradycardia with AV nodal blockade
• Chest radiograph to detect signs of
congestive heart failure and pulmonary
renal syndromes often characterized by
pulmonary alveolar hemorrhage.
• Kidney ultrasonography to determine
kidney sizes (distinguishes acute from
chronic kidney disease), presence of
obstruction, and renal vascular status
(Doppler study)
• Computed tomography (CT) with
radiocontrast administration is typically
avoided in AKI. However, unenhanced CT
scans may identify obstructing ureteral
stones.

AKI Treatment :
TREATMENT OF COMPLICATIONS of ACUTE
RENAL FAILURE:
• Volume overload is managed by:
− Salt restricted to 1–2 gm/day.
− Water intake <500 mL + previous 24 hours
urine output.
− Diuretic—Frusemide and thiazide
− Ultrafiltration and dialysis.
• Hyponatremia is managed by:
− Restriction of water <1 L/day.
− Avoid IV hypotonic solution like dextrose In
severe hyponatremia.
− 3% hypertonic saline infusion.
• Hyperkalemia is managed by:
− Restrict dietary potassium <40 mmol/day.
− Eliminate potassium supplement and
potassium sparing diuretic, fruit and fruit
juice, ACEI/ARB.
− Calcium gluconate or calcium chloride
(10%) 10 mL over 10 minutes (emergency
treatment).
− Slow IV infusion of 50 mL 50% dextrose
with 12 U regular insulin.
− Sodium bicarbonate—50–100 mmol IV
infusion if ARF is associated with acidosis.
− Dialysis or hemofiltration.

AKI Treatment : …
TREATMENT OF COMPLICATIONS of ACUTE:
•Metabolic acidosis is managed by:
− Restrict dietary protein to 0.5 gm/kg/day.
− Inj. Na bicarbonate (50–100 mmol IV) to
maintain pH >7.2 and bicarbonate >15 mmol/L.
Na-bicarbonate 500 mg tds orally.
− Dialysis.
• Hyperphosphatemia is managed by:
− Restrict dietary phosphate <800 mg/day.
− Phosphate binding
• Hypocalcemia is managed by:
− CaCO3—1000–1500 mg/day orally.
• Hypermagnesemia is managed by:
− Discontinue Mg containing antacids.
• Hyperuricemia is managed:
− Usually no treatment is necessary if serum
uric acid <7.0 mg/dL.
− Allopurinal of— 200 mg/day
− Febuxostat 40 to 80 mg/day.
• Nutrition is managed by:
− Restrict dietary protein <0.5 g/kg/day.
− Carbohydrate 100 g/day.
− Enteral/parenteral nutrition.
• Anemia is treated by:
− Packed cell transfusion and injection
erythropoietin by subcutaneous route. 4000 K
on alternate day.
• Renal replacement therapy.

Indication For Dialysis :
• Diuretic resistance—Severe
hypervolemia causing CCF and
pulmonary edema.
• Acidosis—pH <7.2.
• Hyperkalemia—K+ level >7 mcg/L.
• Blood urea >200 mg/dL.
• Plasma creatinine >10 mg/dL.
• Pericardial rub.
• Uremic encephalopathy.
− Dialysis in ARF is initiated earlier
particularly in oliguric and critically ill
patient.
− Stable patient with ARF is expected to
recover renal functions within several days
and may benefit from fluid restriction,
restriction of protein, Na+, K+ and PO4
• Inspite of best treatment, mortality rate is
approximately 60%. Bad prognostic
indicators are:
• Older age group
• Multiorgan failure
• Severe oliguria/anuria at presentation
• High plasma creatinine at presentation
• Cachexia.

Complications of AKI :

CKD Background:
Chronic renal failure (CRF) is a syndrome characterized by gradual suppression of
Glomerular filtration rate (GFR) over weeks to months leading to accumulation of
nitrogenous waste product in the body.
Chronic kidney disease (CKD) is diagnosed when there is evidence for more than 3
months of kidney damage (urine albumin >30 mg/g creatinine, hematuria, or
parenchymal abnormalities) and/or decreased kidney function (glomerular filtration
rate, GFR <60 ml/min/1.73 m2).
CKD is characterized by accumulation of metabolic waste products in blood,
electrolyte abnormalities, mineral and bone disorders, and anemia.

CKD Background: …
Chronic Renal Disease : It is a pathophysiologic process of multiple etiology resulting in
irreversible loss of number and function of nephrons frequently leading to end-stage renal
disease (ESRD).
End-stage Renal Disease : It is a clinical stage of chronic renal disease due to irreversible
loss of renal function to a degree sufficient to render the patient dependent on renal
replacement therapy (dialysis or transplant).
Azotemia : Retention of nitrogenous waste products when renal insufficiency develops.
Uremia : This is a clinical and laboratory syndrome that reflects dysfunction of all organs
due to accumulation of nitrogenous waste product as a result of untreated or undertreated
acute or chronic renal failure.

CKD Pathophysiology:
Manifestation Mechanisms
Accumulation of nitrogenous
waste Products
Decrease in glomerular filtration rate
Acidosis Decreased ammonia synthesis , Impaired bicarbonate reabsorption
Decreased net acid excretion
Sodium retention Excessive renin production, Oliguria
Hyperkalemia Decrease in glomerular filtration rate, Metabolic acidosis, Excessive potassium
intake , Hyporeninemic hypoaldosteronism
Growth retardation Inadequate caloric intake, Renal osteodystrophy , Metabolic acidosis , Anemia
Growth hormone resistance
Anemia Growth hormone resistance, Anemia Decreased erythropoietin production
Iron deficiency , Folate deficiency, Vitamin B12 deficiency, Decreased erythrocyte
survival
Hypertension Volume overload, Excessive renin production
Hyperlipidemia Decreased plasma lipoprotein lipase activity
Pericarditis, cardiomyopathy Uremic factor(s), Hypertension, Fluid overload
Infection Defective granulocyte function, Impaired cellular immune functions
Indwelling dialysis catheters

CKD Causes:
Diabetes (43.2%),
Hypertension (23%),
chronic glomerulonephritis (12.3%)
Failed kidney transplant
Polycystic kidney disease (2.9%)
Interstitial nephritis (e.g., drug hypersensitivity, analgesic nephropathy)
Obstructive nephropathies (e.g., nephrolithiasis, prostatic disease)
Vascular diseases (renal artery stenosis, hypertensive nephrosclerosis)
Autoimmune diseases

CKD Risk Factors :

CKD Sign & Symptoms :
PHYSICAL FINDINGS & CLINICAL PRESENTATION:
Skin pallor, ecchymosis.
Sleep disorder.
Hypertension.
Edema, leg cramps, restless legs, peripheral neuropathy.
Emotional lability, depression, decreased cognitive function.
Clinical presentation varies with the degree of kidney disease and its underlying
etiology.
Common symptoms are generalized fatigue, nausea, anorexia, pruritus, sleep
disturbances, smell and taste disturbances, hiccups, and seizures.

CKD Sign & Symptoms : …

CKD Stages :

CKD Investigations :

AKI & CKD :

CKD :

CKD Treatment :

Differences between AKI & CKD :

THANK YOU

Renal failure by dr hari sharan aryal

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