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RENAL
FAILURE
ROLL NO :- 1 -
10
OBJECTIVES OF THE SEMINAR
Anatomy and physiology of kidney
Biochemical aspects of kidney
The prevalence, risk factors, epidemiology of kidney of
kidney diseases
Etiology and etiological agents causing kidney damage
Pathology of renal failure
Pharmacotherapy & management of renal failure
Clinical Case
CLINICAL CASE
Sajid Aalam
Roll No : 01
CLINICAL CASE
Chief Complaint: A 62-year-old male
presented to the emergency department with
complaints of increasing weakness, fatigue,
and shortness of breath for the past week.
He reported a decreased urine output and
swelling of his legs
On examination: The patient appeared pale
and visibly fatigued. Blood pressure was
170/100 mmHg, and heart rate was 90 beats
per minute. The abdomen was distended, and
there was bilateral pitting edema in the lower
extremities. Heart sounds were regular with no
murmurs.
Past History: The patient had a past medical
history significant for hypertension, type 2
diabetes mellitus, and dyslipidemia. He also
had a history of heavy alcohol consumption,
smoking, and a sedentary lifestyle
Lab Findings:
Blood tests show:
1. Serum Creatinine = 9.5 mg/dL
2. Blood Urea Nitrogen = 90 mg/dL
3. Potassium = 6.5 mmol/L
4. Serum Albumin = 2.5 g/dL
5. Hemoglobin = 9 g/dL
Urine output = 50 ml/24 hours.
Anatomy
ANATOMY OF KIDNEY
Sameer Adhikari
Roll No : 5
Features & Location
Bean shaped
Posterior abdominal wall
11cm long , 6 cm broad and 3 cm thick
T12-L3
Right Kidney is lower than Left Kidney
Occupies Epigastric, hypochondrium,
lumbar and umbilical regions
External Features
Poles
 Upper
 Lower
Surfaces
 Anterior
 Posterior
Borders
 Lateral
 Medial
Hilum
Covering Of Kidney
 Paranephric fat
 Renal fascia
 Perinephric fat (adipose
capsule)
 True capsule of kidney
Kidney – Coronal Section
Outer Cortex
Inner Medulla
• Renal pyramid
• Renal papillae
• Renal column
• Minor calyx
• Major calyx
Renal Sinus
• Renal vein
• Renal artery
• Renal pelvis
Found the missing part
Left kidney:
i. Suprarenal area
ii. Splenic area
iii. Gastric area
iv. Pancreatic area
v. Jejunal area
vi. Colic area
Anterior Relation Of Kidney
Right kidney:
i.Suprarenal area
ii. Duodenal
iii. Hepatic area
iv. Colic area
v. Jejunal area
NEPHRON- Functional Unit
Glomerulus
Bowman’s Capsule
Proximal Convulated Tubules
Loop of Henle
Distal Convulated Tubules
Collecting Ducts
Arterial Supply
Renal artery- fromAA
Divides into anterior and
posterior trunks
Anterior trunk -
 Apical
 Upper and anterior (anterosupeior)
 Middle and anterior (anteroinferior)
 Inferior
Posterior Trunk
 Behind the renal pelvis
 Continue as posterior segmental artery
Vascular Segments
Apical
Caudal
Anterior Superior
Anterior Inferior
Posterior
Venous drainage
Lymphatic drainage
Lateral aortic lymph nodes
Nerve supply:
Renal plexus- coeliac plexus
Sympathetic fibers- T10- L1
 Parasympathetic- Vagus Nerve
Physiology
PHYSIOLOGY OF KIDNEY
PRABEJ ALAM
Roll No : 06
NEPHRON
URINE FORMATION
Glomerular Filtration Rate (GFR)
 Rate of blood filtered
100-120 /ml /min /1.73 m2
Less in female
Less with ageing
FUNCTIONS OF KIDNEY
Excretory function
Homeostatic function
Endocrine function
Metabolic function
Excretory Function
By forming urine, the kidneys help excrete waste
substances that have no useful functions in the body
Some wastes excreted in urine
Ammonia and Urea
Bilirubin
Creatinine
Uric acid
Homeostatic Function
 Corrects any acid base
imbalance by :
 Removing excess
acid ( hydrogen ion)
or bases
(bicarbonates) in the
urine and
 Restoring the
bicarbonate
concentration in the
blood to normal
Regulation of blood pressure – RAAS System
Regulation of Osmolarity
and blood volume
 osmoreceptors signalling
pathway
Water deficit
Extracellular osmolarity
ADH secretion
(posterior pituitary)
Plasma ADH
H20 permeability in distal
tubule, collecting ducts
H2O reabsorption
H2O excreted
Osmoreceptors
Endocrine Function
Two hormones :
 Erythropoietin (EPO)
 Calcitriol (1,25[OH]2 Vitamin D3
Erythropoietin
 Acts on bone marrow to increase the production of RBC
 Stimuli such as bleeding or moving to high altitudes(where oxygen
is scarer) trigger the release of EPO
 Without a source of EPO, people with failing kidneys; dialysis
suffer from anaemia
Calcitriol
 It acts on :
 Cells of intestine to promote the absorption of calcium and phosphate
from food
 Bone to mobilize calcium from the bone to the blood
Metabolic Function
 Regulation of blood glucose level
 Gluconeogenesis - kidneys can use the amino acid glutamine in
gluconeogenesis, the synthesis of new glucose molecule
 They can then release glucose into the blood to help maintain a normal
blood glucose level
RENAL FUNCTION TEST
 Glomerular Function Test
 Tubular Function Test
 Analysis Of Blood / Serum
 Urine Examination
Glomerular Function Test
 Measures GFR
 GFR = Amount of blood filtered per minute by kidney
 It includes
 Creatinine Clearance =120-140 ml/min
 Urea Clearance = 75 ml/min
Tubular Function Test
 Measures functions of tubules to concentrate urine
 It includes
 Urine Concentration Test
Normal urine specific gravity = 1.020
 Osmolality Test
Normal osmolality = 500 – 1200 milliosmoles / kg
Analysis Of Blood / Serum
Estimates the clearance of substances from serum
Substance measured are
 Serum creatinine = 0.7 – 1.3 mg/dl ( male)
= 0.5 – 1.1 mg/dl ( female )
 Blood Urea = 10 – 40 mg/dl
 Serum Cystatin c = 0.8 – 1.2 mg/dl
Urine Examination
Acute Kidney
Injury
ACUTE KIDNEY INJURY
(AKI)
ASHISH BARAL
Roll No : 08
 Sudden impairment of kidney function
 Occurring over hours to days
 Resulting in the retention of nitrogenous and other
waste products
DEFINITION
EPIDEMIOLOGY
 5–7% of acute care hospital admissions
 30% of admissions in ICU
 Major medical issue of developing countries
 worldwide -13.3 million cases
- 1.7 million deaths/year
 etiologies - region specific
- species of snakes, spiders, bees
- malaria, leptospirosis
GLOBAL INCIDENCE
South
America
31%
Southeast
Asia 31%
South
Asia
7.5%
INCIDENCE IN NEPAL
Major health issue-rural areas
As per the WHO :
• 10% of population - suffering from renal problems
• 30,000 - final stage of kidney failure and
• 3,000 - suffer from kidney failure every year
CAUSES OF AKI
Pre renal
Intrinsic renal
Post renal
Sudden and severe reduction in blood flow
to the kidney
• Blood loss
• Dehydration
• Heart failure
• Sepsis
• Vascular occlusion
Pre renal
Direct injury to the kidney
• Acute tubular necrosis
• Acute interstitial nephritis
• Glomerular nephritis
Intrinsic renal
Sudden obstruction to flow of urine
• Kidney stones
• Bladder injury/tumor
• Enlarged prostate
• Urethral stricture
Post renal
RISK FACTORS
MODIFIABLE NON-MODIFIABLE
Hypercholesterolemia Age (above 65)
Hypertension Kidney disease
Hypoalbuminemia Congestive heart failure
Dehydration Diabetes mellitus
Sepsis AIDS
Rhabdomyolysis Renal artery stenosis
Nephrotoxic drugs use Peripheral vascular disease
Pathogenesis
Clinical Features
PATHOGENESIS &
CLINICAL FEATURES OF AKI
Keshav Acharya
Roll No : 03
PATHOGENESIS
Pre Renal
Renal
Post Renal
Pre renal
Renal
 Rapidly Progressive Glomerulonephritis (RPGN)
 Acute Tubular Necrosis(ATN)
 Acute Interstitial Nephritis e.g. Infections, drugs , toxins,
sarcoidosis, amyloidosis
Post Renal
CLINICAL PRESENTATION
Clinical presentation With Specific complications
 Hypovolemia
 Hypervolemia / Fluid overload
 Hyperkalemia
 Hypokalemia
 Uremia
Clinical Presentation In General
Clinical Presentation In General
Rash
Fever
Eosinophilia
Anuria
Hematuria
Foamy urine
Clinical Presentation With Hypovolemia
Symptoms:
 Dizziness
 Fatigue
 Confusion
 Decreased urine output
Physical examination findings:
 Hypotension tachycardia
 Poor skin turgor
 Dry mucous membrane
Clinical Presentation With Hypervolemia
 Symptoms:
 Dyspnea
 Abdominal distension
 Swelling in the extremities
 Physical examination findings:
 Edema
 Crackles
 Ascites
 Pleural effusion
 Elevated JVP
 S3 heart sound
Clinical Presentation With Hyperkalemia
Symptoms
 Severe muscle weakness
 Paralysis
 Cardiac conduction abnormalities
• RBBB
• LBBB
• Advanced atrioventricular block
• Arrythmias
Clinical Presentation With Hypokalemia
Symptoms
 Muscle cramps
 Ileus
Physical examination findings
 Usually normal
 May have muscle weakness with rhabdomyolysis, if severe
 ECG changes
Clinical Presentation With Uremia
Symptoms
 GI:
 Anorexia
 Nausea/vomiting
 Dysgeusia
 Neurologic:
 Confusion
 Drowsiness
 Encephalopathy
 Seizure
 Coma
Physical examination findings
 Asterixis
 Myoclonus
 Pericarditis
 pericardial effusion
Myoclonus
DIAGNOSIS,
MANAGEMENT &
COMPLICATIONS
DIAGNOSIS, MANAGEMENT
& COMPLICATIONS of AKI
Binayak Baral
Roll No : 09
DIAGNOSTIC EVALUATION
Urine Test
Blood Test
Imaging Techniques
Kidney Biopsy
Urine Tests
Urine output = <200 ml/6 hours
Hematuria
Proteinuria
↓ specific gravity.
Hyponatremia (below 20 mEq/L) in urine
BUN = Elevated
Serum creatinine increases (>0.3mg/dl in 48hrs)
Hyperkalemia
↓ bicarbonate level
↓ hematocrit and Hemoglobin
Low blood pH
Electrolyte level imbalance
Complete blood count for infections
Blood Tests
Imaging Tests
Ultrasonography
KUB radiography
MRI
Pyelography
Computerized
Tomography(CT)
Pyelography
USG of kidney showing Hydronephrosis
Kidneys, Ureters, Bladder
(KUB) radiograph showing
calculus
Kidney Biopsy
 Kidney biopsy is done as a last resort of diagnosis of Acute renal
failure
Acute tubular necrosis
MANAGEMENT
Treatment for acute kidney failure varies according to
underlying cause
Goal of treatment is to :
 Correct or treat the cause of kidney failure
 Restore kidney function and
 Prevent fluid and waste from building up
Pharmacologic Therapy
Optimization of systemic and renal hemodynamics
 Antihypertensive
 Diuretics
Elimination of nephrotoxic agents(NSAIDs,
aminoglycosides)
 Diuretics
 Hyperkalemia
 Discontinuation of potassium-sparing diuretics, ACE
inhibitors, ARBs, NSAIDs
 Loop diuretics to promote urinary potassium loss
Metabolic acidosis
 Sodium bicarbonate (if pH <7.2 , serum bicarbonate >15 mmol/L)
Infections
 Antibiotics erythromycin, azithromycin, chloramphenicol
Dialysis to remove toxins from the blood
COMPLICATION
Fluid buildup in lungs
Muscle weakness, paralysis
Cardiac complications
Infections
Acidosis
Permanent kidney damage
AKI can lead to loss of kidney function and ,ultimately death
CHRONIC KIDNEY
DISEASES (CKD)
CHRONIC KIDNEY DISEASES
(CKD)
Bishal Banmala
Roll No : 07
DEFINITION
Subtle ↓ kidney function
Develops over a minimum 3 months
Renal function are compromised
↓ GFR, ↓ Renal output
EPIDEMIOLOGY
Public health problem worldwide
Incidence and prevalence increasing
Prevalent in older adults, males, americans
Us prevalence -15%
Europe prevalence 3% to 17%
GLOBAL INCIDENCE
RISK FACTORS
Advanced age
Family history
Systemic inflammation
Dyslipidemia
ETIOLOGY
Initiation
 Diabetes
 Hypertension
 Glomerulonephritis
Progression
 Hyperglycemia
 Proteinuria
 Obesity
Lumen of renal artery decreased,
less oxygen supply
Glomerulus sclerosis/Chronic kidney
disease
Mesangial Cells -Mesoangioblasts -
Extracellular Matrix
TGF-B1 release
Ischemia , immune cell activated
Glomerulus sclerosis gross Glomerulus sclerosis Histology
Non enzymatic glycation
occurs in efferent
arteriole
Stiffness and narrowing of
efferent arteriole
Glomerulus sclerosis
PATHOGENESIS
& STAGES
PATHOGENESIS & STAGES
of CKD
Prashant Basel
Roll No : 10
Initiating factor
Hypertension, diabetes, toxin exposure,
immune complex deposition, autoimmune
disease etc.
Decrease number & function of
nephrons
PATHOGENESIS
 Aging = nephron number
STAGES OF CKD
Stage 5 CKD: End Stage Renal Disease (ESRD)
Inability of kidney to function completely
Accumulates toxin, fluids, electrolyte
Disturb water, electrolyte homeostasis
CLINICAL FEATURES
&
DIAGNOSIS
CLINICAL FEATURES &
DIAGNOSIS OF CKD
Anurag Acharya
Roll No : 02
CLINICAL FEATURES
Azotemia Followed By Uremia
Electrolyte Imbalance
Hematopoietic System
Gastrointestinal Tract
Urinary System
CVS
Azotemia Followed By Uremia
 General symptoms
 Nausea
 Loss of appetite
 Burning urination
 CNS
 Encephalopathy
 Coma and even death
 CVS
 Pericarditis
 Bleeding – platelets don’t stick, and no clot is formed.
 Skin
 Uremic Frost
Electrolyte Imbalance
 Potassium imbalance
Hyperkalemia  Cardiac arrhythmia
 Calcium imbalance
less activated Vitamin D  Hypocalcemia  PTH hormones
act Renal osteodystrophy
 Sodium imbalance
sodium & water retained  HTN, Edema
Hematopoietic System
Impaired Erythropoiesis
 Due to less erythropoietin
 Lower production of RBC
 Finally, anemia
Gastrointestinal Tract
Mucosal ulcerations
GI bleeding
Stomatitis
Urinary System
Polyuria = Inability of kidney to concentrate urine
Oliguria
Anuria
CVS
 Low fluid filtered  Renin  HTN
HTN CKD
DIAGNOSIS OF CKD
History
 ≥ 3 months of Kidney injury
GFR
 Normal= 125ml/min
 Can be estimated by : (i) Creatinine test
(ii) Cystatin C test
Albuminuria
Polycystic Kidney Disease
Renal Ultrasonography
Renal Biopsy
1. Complete Blood Count
RBC  Decreased  Anemia (normocytic,
normochromic)
2. Parathyroid level  Increased
3. Basic Metabolic Panel(BMP) test
K+ and Na+  Increased
4. Arterial Blood Gas(ABG) Analysis
H+  Increased (metabolic acidosis)
5. Lipid panel test
Triglyceride and LDL  Increased
Other Lab Investigations
MANAGEMENT
MANAGEMENT OF CKD
Laxman Acharya
Roll No : 04
THERAPEUTIC MANAGEMENT
Managing complications
 Disorders Of Calcium And Phosphate Metabolism
 Cardiovascular Abnormalities
 Hematological Abnormalities
 Neuromuscular Abnormalities
 Medication Dose Adjustment
 Renal Replacement Therapy
Disorders Of Calcium And Phosphate Metabolism
low phosphate diet
Use of phosphate binding agents
Use of calcitriol
Cardiovascular Abnormalities
Management of hypertension
 Salt restrictions
 Antihypertensive agents like ARBs ACE inhibitors
Hematological Abnormalities
 Anemia
 Recombinant human Erythropoietin Stimulating Agents
therapy
Neuromuscular Abnormalities
 Peripheral neuropathy is an indication to start Renal Replacement
therapy
Medication Dose Adjustment
 Loading dose not affected by CKD.
 Maintenance doses need to be adjusted
Renal Replacement Therapy
 why is it required ?
 What are the indications for
initiation of Renal
Replacement Therapy ?
 Treatment options for
patients with ESRD ?
after renal
replacement
DIALYSIS
Hemodialysis
Peritoneal dialysis
TRANSPLANTATION OF KIDNEY
 Treatment of choice with ESRD
 Types
 Living donor kidney transplant
 Deceased donor kidney transplant
 Transplant rejection ?
SUMMARY
SUMMARY
&
CLINICAL CASE DIAGNOSIS
Sajid Aalam
Roll No : 01
So did you all understand
renal failure ??
or
SUMMARY
Several etiological factors
Acute renal injury Chronic renal disease
Resolve
End stage renal disease
Death
Normal kidneys
THE CASE…
Chief Complaint : A 62-year-old male presented to the emergency
department with complaints of increasing weakness, fatigue, and shortness
of breath for the past week. He reported a decreased urine output and
swelling of his legs.
 On examination: the patient appeared pale and visibly fatigued. Blood
pressure was 170/100 mmHg, and heart rate was 90 beats per minute. The
abdomen was distended, and there was bilateral pitting edema in the
lower extremities. Heart sounds were regular with no murmurs.
Past History : The patient had a past medical history significant for
hypertension, type 2 diabetes mellitus, and dyslipidemia. He also reported
a history of heavy alcohol consumption, smoking, and a sedentary
lifestyle.
Blood tests show:
1. Serum Creatinine = 9.5 mg/dL
2. Blood Urea Nitrogen = 90 mg/dL
3. Potassium = 6.5 mmol/L
4. Serum Albumin = 2.5 g/dL
5. Hemoglobin = 9 g/dL
Urine output = 50 ml/24 hours
Laboratory Findings :
DIAGNOSIS ?
Q & A
Failed FNT is better than a failed kidney
but I know we can pass both
so
study enough & drink enough!
HAVE A GOOD DAY!
water
Renal Failure

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