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CHRONIC KIDNEY DISEASE
BY
MOHAMMED SHADAB
16901087
MBBSYR 5
OUTLINE OFTHE PRESENTATION
• DEFINITION
• RISK FACTORS
• PATHOGENESIS AND STAGES
• CLINICAL FEATURES
• LABVALUES
• PREVENTION AND
MANAGEMENT
• LATEST UPDATES / RESEARCH
• SOURCES OF PRESENTATION
Definition
• Progressive, irreversible loss of
renal function in the presence of
kidney damage resulting in a
decline of GFR < 60 ml/hour for
at least 3 months.
• •Main causes : Diabetes Mellitus
& Hypertension
• •GFR < 15 ml/hour indicates a
late stage and is called ESRD
(CKD STAGE 5)
IN the UAE:
-Among Emiratis, 4.6% of males and
2.8% of females
-Among expatriates, 4.2% of males and
3.2% of females
Ref- Richards N, Hassan M, Saleh AK, Dastoor H, Bernieh B,
Abouchacra S, et al. Epidemiology and referral patterns of
patients with chronic kidney disease in the Emirate of Abu
Dhabi. Saudi J Kidney DisTransplant Off Publ Saudi Cent
OrganTransplant Saudi Arab. 2015;26: 1028–1034.
doi: 10.4103/1319-2442.164600 [PubMed]
CLINICAL FEATURES
• Uremia
• Urinary symptoms : Polyuria, Nocturia, Isosthenuria (Fixed urine SG of 1.010 = RT damage Failure of
concentration) Oliguria Anuria
• Metabolic disturbances due to accumulation if waste products Nausea, vomiting, headache, impaired cognition
• Metabolic acidosis
• Erythropoietin deficiency
• Reduced immunity (Immunosuppression) & altered WBC function Infections, fever; Bleeding tendency due to
reduced Platelet function
• CVS : RAAS activation Hypertension LVH 1. Atrial fibrillation 2. CHF 3. Angina pectoris & AMI; Uremic
pericarditis (Inflammatory)
• Respiratory : Uremic Pleuritis
• GIT : Mousy odour of urea in breath “Uremic fetor”
• CNS: Altered cognition, Seizures, Coma.
• “Renal rickets”
• Peripheral neuropathy : Restless Leg Syndrome
What to expect in investigations
• URINE : Low fixed SG 1.010, (1.015 – 1.025) and Proteinuria
• Urine culture (UTI : Immunosuppression, catheter related, related to DM);
• •BLOOD: Low Hb Anemia (Low Erythropoietin) Reduced HCT;
• CXR : Cardiomegaly + Tendency for vascular congestion due to increased capillary
permeability (“Uremic lung”)
• ECG : LVH. Atrial fibrillation, Changes due to high K+, Changes due to low or high calcium
• Ultra sound Abdomen: Bilateral shrunken kidneys.
Unilateral small kidney ??
Fluid & Electrolyte disturbances
• Na+ : may ne normal / Low. Na+ retention can lead to H2O retention
Edema, Hypertension, CHF .
• K+ : Hyperkalemia : Most dreaded Fatal arrhythmias.
• PO4 : Initial PO4 retention may result in Hyperphosphatemia
Hypocalcemia
• Ca+ : May be Low (Initial Due to PO4 retention) or High (later due to Hyper
Parathyroidism –Primary / Tertiary
Renal
osteodystrophy
MANAGEMENT
HYPERTENSION : Goal BP 130/80 mmHg. Preferred drug ACEI / ARB
•Renal osteodystrophy : Hyperphosphatemia –Restricting PO4 intake to < 1000mg; PO4 binders Calcium
carbonate (Tums)
Vit D supplementation : Calcitriol-Serum PO4 level must be lowered before giving Vit D or Calcium
Controlling Hyper PTH : Cinacalcet
•Anemia : Erythropoietin alpha Scor IV, Iron (if Ferritin < 100 ) Folic acid (if patient is on dialysis –as FA is
removed by dialysis; No role for blood transfusion
DRUGSTO AVOID
• Avoid NSAID
• •Be careful with Digitalis
• •Be careful while selecting antibiotics
Disequilibrium syndrome
• : Hemodialysis Rapid reduction in Plasma osmolarity +
Comparably less rapid reduction in brain osmolarity -
Cerebral edema Nausea, vomiting, twitching,
convulsions, coma. Usually at the end of first and second
dialysis
Research
• Researchers have been working on ways to grow healthy organs outside the human
body.
• Blastocyst complementation, has already produced promising results
• blastocysts, the clusters of cells formed several days after egg fertilization, from mutant animals missing
specific organs and inject them with stem cells from a normal donor, not necessarily of the same species.
• The stem cells then differentiate to form the entire missing organ in the resulting animal.
• The new organ retains the characteristics of the original stem cell donor, and can potentially be used in
transplantation therapy
About the Experiment
• Researchers first tried to grow rat kidneys in mice  was unsuccessful
• rat stem cells did not differentiate into the two main types of cells needed for kidney
formation.
• When they reversed the scenario
• mouse stem cells differentiated inside rat blastocysts, forming the basic structures of a
kidney.
• After being implanted into pseudo-pregnant rats
• the complemented blastocysts matured into normal fetuses.
• more than two thirds of the resulting rat neonates contained a pair of kidneys derived from
the mouse stem cells.
• Further screening showed that all of the kidneys were structurally intact, and at least half
could potentially produce urine
REFERENCE
• Davidson’s Principles and Practice of Medicine 23rd edition, Chapter 17-Kidney and Urinary tract
diseases.
• Kumar and Clark’s Clinical Medicine, 7th Edition, Chapter 11-Renal diseases
• Netter’s Internal Medicine, 2nd Edition, , Chapter 14- Disorders of Kidney and Urinary tract
• Harrison’s Principles of Medicine ,19th Edition, Part 13, Chapter 335 – Chronic Kidney Diseases.
• Richards N, Hassan M, Saleh AK, Dastoor H, Bernieh B, Abouchacra S, et al. Epidemiology and
referral patterns of patients with chronic kidney disease in the Emirate of Abu Dhabi. Saudi J
Kidney Dis Transplant Off Publ Saudi Cent Organ Transplant Saudi Arab. 2015;26: 1028–1034.
doi: 10.4103/1319-2442.164600 [PubMed]
• Dr. RAGHVENDRA BHAT ( MD, FRCP (glasg) Professor Internal Medcine)YR 4 LECTURE
• GUFRAN AL HILFI
• 16901073
•(latest research details)
THANKYOU

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Chronic kidney disease

  • 1. CHRONIC KIDNEY DISEASE BY MOHAMMED SHADAB 16901087 MBBSYR 5
  • 2. OUTLINE OFTHE PRESENTATION • DEFINITION • RISK FACTORS • PATHOGENESIS AND STAGES • CLINICAL FEATURES • LABVALUES • PREVENTION AND MANAGEMENT • LATEST UPDATES / RESEARCH • SOURCES OF PRESENTATION
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  • 4. Definition • Progressive, irreversible loss of renal function in the presence of kidney damage resulting in a decline of GFR < 60 ml/hour for at least 3 months. • •Main causes : Diabetes Mellitus & Hypertension • •GFR < 15 ml/hour indicates a late stage and is called ESRD (CKD STAGE 5)
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  • 6. IN the UAE: -Among Emiratis, 4.6% of males and 2.8% of females -Among expatriates, 4.2% of males and 3.2% of females Ref- Richards N, Hassan M, Saleh AK, Dastoor H, Bernieh B, Abouchacra S, et al. Epidemiology and referral patterns of patients with chronic kidney disease in the Emirate of Abu Dhabi. Saudi J Kidney DisTransplant Off Publ Saudi Cent OrganTransplant Saudi Arab. 2015;26: 1028–1034. doi: 10.4103/1319-2442.164600 [PubMed]
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  • 11. CLINICAL FEATURES • Uremia • Urinary symptoms : Polyuria, Nocturia, Isosthenuria (Fixed urine SG of 1.010 = RT damage Failure of concentration) Oliguria Anuria • Metabolic disturbances due to accumulation if waste products Nausea, vomiting, headache, impaired cognition • Metabolic acidosis • Erythropoietin deficiency • Reduced immunity (Immunosuppression) & altered WBC function Infections, fever; Bleeding tendency due to reduced Platelet function • CVS : RAAS activation Hypertension LVH 1. Atrial fibrillation 2. CHF 3. Angina pectoris & AMI; Uremic pericarditis (Inflammatory) • Respiratory : Uremic Pleuritis • GIT : Mousy odour of urea in breath “Uremic fetor” • CNS: Altered cognition, Seizures, Coma. • “Renal rickets” • Peripheral neuropathy : Restless Leg Syndrome
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  • 13. What to expect in investigations • URINE : Low fixed SG 1.010, (1.015 – 1.025) and Proteinuria • Urine culture (UTI : Immunosuppression, catheter related, related to DM); • •BLOOD: Low Hb Anemia (Low Erythropoietin) Reduced HCT; • CXR : Cardiomegaly + Tendency for vascular congestion due to increased capillary permeability (“Uremic lung”) • ECG : LVH. Atrial fibrillation, Changes due to high K+, Changes due to low or high calcium • Ultra sound Abdomen: Bilateral shrunken kidneys. Unilateral small kidney ??
  • 14. Fluid & Electrolyte disturbances • Na+ : may ne normal / Low. Na+ retention can lead to H2O retention Edema, Hypertension, CHF . • K+ : Hyperkalemia : Most dreaded Fatal arrhythmias. • PO4 : Initial PO4 retention may result in Hyperphosphatemia Hypocalcemia • Ca+ : May be Low (Initial Due to PO4 retention) or High (later due to Hyper Parathyroidism –Primary / Tertiary
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  • 18. HYPERTENSION : Goal BP 130/80 mmHg. Preferred drug ACEI / ARB •Renal osteodystrophy : Hyperphosphatemia –Restricting PO4 intake to < 1000mg; PO4 binders Calcium carbonate (Tums) Vit D supplementation : Calcitriol-Serum PO4 level must be lowered before giving Vit D or Calcium Controlling Hyper PTH : Cinacalcet •Anemia : Erythropoietin alpha Scor IV, Iron (if Ferritin < 100 ) Folic acid (if patient is on dialysis –as FA is removed by dialysis; No role for blood transfusion
  • 19. DRUGSTO AVOID • Avoid NSAID • •Be careful with Digitalis • •Be careful while selecting antibiotics
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  • 21. Disequilibrium syndrome • : Hemodialysis Rapid reduction in Plasma osmolarity + Comparably less rapid reduction in brain osmolarity - Cerebral edema Nausea, vomiting, twitching, convulsions, coma. Usually at the end of first and second dialysis
  • 22. Research • Researchers have been working on ways to grow healthy organs outside the human body. • Blastocyst complementation, has already produced promising results • blastocysts, the clusters of cells formed several days after egg fertilization, from mutant animals missing specific organs and inject them with stem cells from a normal donor, not necessarily of the same species. • The stem cells then differentiate to form the entire missing organ in the resulting animal. • The new organ retains the characteristics of the original stem cell donor, and can potentially be used in transplantation therapy
  • 23. About the Experiment • Researchers first tried to grow rat kidneys in mice  was unsuccessful • rat stem cells did not differentiate into the two main types of cells needed for kidney formation. • When they reversed the scenario • mouse stem cells differentiated inside rat blastocysts, forming the basic structures of a kidney. • After being implanted into pseudo-pregnant rats • the complemented blastocysts matured into normal fetuses. • more than two thirds of the resulting rat neonates contained a pair of kidneys derived from the mouse stem cells. • Further screening showed that all of the kidneys were structurally intact, and at least half could potentially produce urine
  • 24. REFERENCE • Davidson’s Principles and Practice of Medicine 23rd edition, Chapter 17-Kidney and Urinary tract diseases. • Kumar and Clark’s Clinical Medicine, 7th Edition, Chapter 11-Renal diseases • Netter’s Internal Medicine, 2nd Edition, , Chapter 14- Disorders of Kidney and Urinary tract • Harrison’s Principles of Medicine ,19th Edition, Part 13, Chapter 335 – Chronic Kidney Diseases. • Richards N, Hassan M, Saleh AK, Dastoor H, Bernieh B, Abouchacra S, et al. Epidemiology and referral patterns of patients with chronic kidney disease in the Emirate of Abu Dhabi. Saudi J Kidney Dis Transplant Off Publ Saudi Cent Organ Transplant Saudi Arab. 2015;26: 1028–1034. doi: 10.4103/1319-2442.164600 [PubMed] • Dr. RAGHVENDRA BHAT ( MD, FRCP (glasg) Professor Internal Medcine)YR 4 LECTURE
  • 25. • GUFRAN AL HILFI • 16901073 •(latest research details)