CKD. CHRONIC KIDNEY DISEASE presentation for Undergraduates

1. CHRONIC KIDNEY DISEASE
AMANYIRE DICKSON
BMS/7925/163/DU
KIU-WC
SUPERVISOR
DR. MUYINDA ASAD
CARDIOLOGIST
17th FEB, 2023

2. CHRONIC KIDNEY DISEASE
» Decline in the GFR over months to years.
» Persistent proteinuria or abnormal renal morphology may
be present.
» Hypertension in most cases.
» Symptoms and signs of uremia when nearing end-stage
disease.
» Bilateral small or echogenic kidneys on ultrasound in
advanced disease
ESSENTIALS FOR DIAGNOSIS

3. Definition
 Chronic kidney disease is defined as either
kidney damage or GFR < 60 mL/min/1.73 m2
for 3 or more months.
 Kidney damage is defined as pathologic
abnormalities or markers of damage, including
abnormalities in blood or urine tests or
imaging studies.

4. GFR
Measured by Cock-croft Gault formula
GFR(ml/min)= (1.23 x Wt in kgs) x (140-Age) in Males
Creatinine
= (1.03 x Wt in kgs) x (140-Age) in females
Creatinine

5. Staging of CKD
3. At all stages, persistent albuminuria confers added risk for chronic kidney disease
progression and cardiovascular disease in the following; gradations: < 30 mg/day = lowest
added risk, 30–300 mg/day = mildly increased risk, > 300–1000 mg/day = moderately
increased risk, > 1000mg/day = severely increased risk.

6. Aetiology of CKD

7. Reversible causes of CKD

8. Risk factors for faster progression
 ↑ proteinuria
 Higher blood pressure
 ↓ HDL
 Smoking
 Alcohol use
 Poor control of DM
 NSAIDS
 Obesity
 None modifiable:
 Race,
 Old age
 Primary kidney disease

9. Pathophysiology
 CKD leads to progressive decline in RF even if inciting
cause is removed.
 1° insult causing loss of kidney – loss of Nephrons
 Destruction of nephrons leads to compensatory
hypertrophy and supranormal GFR of remaining nephrons
inorder to maintain homeostasis
 However, compensatory hyperfiltration leads to overwork
injury in the remaining nephrons → progressive
glomerular sclerosis and intersistial fibrosis

10. Pathophysiology
Consequently;
 Retention of nitrogenous waste products:
urea → Uremic syndrome
 Impairment of metabolic and endocrine
kidney function resulting in symptoms
 Anemia
 Metabolic bone disorders etc…..

11. Presentation of CKD -Symptoms
Uremic syndrome
 Fatigue,
 Anorexia,
 Nausea,
 Metallic mouth taste
Neurologic symptoms:
 Memory impairment,
 Insomnia,
 Restless legs
 Twitching
 Generalised pruritus (no rash
 Decreased libdo,
 Menstrual irregularities.
 Pericarditis may present with
pleuritic chest pain
 Increased drug toxicity of
drugs eliminated by the
Kidneys: eg increased risk of
hypoglycemia from insulin
administration.
Stages 1-4 CKD are asymptomatic until marked GFR ↓

12. Presentation of CKD
 Most common clinical finding is hypertension
 Edema, discolored urine, Flank pain
 Generally sallow appearance
 Halitosis (Uremic fetor)
 Uremic encephalopathy:
 Decreased mental status,
 Asterixis, myoclonus and
 Possibly seizures

13. Screening & early detection
 Justified because there are effective interventions
that can slow disease progression
 Mass screening not recommended
 High risk group to be screened include:
– DM
– HTN
– HIV
– Recovery from AKI
– Family history of CKD
– Systemic infections, UTI, urinary stones- hx of UT obstruction
– Neoplasia
– Auto immune disease
– Patients on nephrotoxic drugs
– Any hospitalized patients

14. Screening
Urinalysis:
protein
RBC,WBC
Serum
creatinine
Kidney US

15. Screening
 Urine: First morning or a random "spot" urine
 Normal urine albumin < 20 mg/day (15 µg/min)
 Between 30 and 300 mg/day - microalbuminuria.
 Urinary albumin-to-creatinine ratio > 30 mg/g implies
albumin excretion is > 30 mg/day
 Albuminuria is persistent albumin excretion > 300
mg/day.

16. Lab evaluation for patients of CKD
 Serum creatinine to estimate GFR
 Albumin to creatinine ratio on morning spot
urine.
 Dipstick exam for RBS’s , WBC’s/sediment
exam
 Ultrasound of the kidneys: size, echogenicity,
Corticomedullary differentiation, evidence of
obstruction
 Serum electrolytes( Na, K, Cl, HCO3)

17. Imaging - USS
 Small echogenic kidneys bilaterally(<9-10cm)
suggests chronic scarring in advanced CKD
 Large kidneys in
 Adult polycystic kidney disease
 Diabetic nephropathy
 HIV-associated nephropathy
 Plasma cell myeloma
 Amylodosis
 Obstructive uropathy

18. Compications of CKD
A. Cardiovascular Complications
 Hypertension
 Coronary artery disease
 Heart failure
 Atrial fibrillation
 Pericarditis
B. Metabolic Bone Disease (MBD)
C. Hematologic Complications
 Anemia
 Coagulopathy

19. Compications of CKD - (MBD)

20. Compications of CKD
D. Hyperkalemia
E. Acid-Base Disorders
F. Neurologic Complications
G. Endocrine Disorders

21. Compications of CKD

22. Management of CKD
Patients with chronic kidney disease should be evaluated
to determine:
 Diagnosis (type of kidney disease)
 Comorbid conditions
 Severity, assessed by level of kidney function;
 Complications, related to level of kidney function;
 Risk for loss of kidney function
 Risk for cardiovascular disease.

23. Management of CKD
 Treatment of reversible causes of renal dysfunction
 Preventing or slowing the progression of renal
disease
 Treatment of the complications of renal dysfunction
 Identification and adequate preparation for RRT

24. Treat Reversible causes of
progression
 Renal hypoperfusion:
 Hypovolemia, hypotension, infection and the
administration of drugs which lower the GFR
(NSAIDS)
 Nephrotoxic drugs
 UTI
 UT obstruction

25. Treatment of CKD
 Specific therapy, based on diagnosis
 Evaluation and management of comorbid
conditions
 Prevention and treatment of CVD
 Preparation for kidney replacement therapy
 RRT (dialysis and transplantation) if signs and
symptoms of uremia are present.

26. Slowing Progression
 Treatment of the underlying cause is vital.
 Aggressive control of diabetes mellitus
 Blood pressure control
 Agents blocking RAAS useful in proteinuric CKD
 Obese patients encouraged to lose weight
 Risks of AKI avoided e.g longterm use of NSAIDS
 Treatment of metabolic acidosis
 SGLT2 important in slowing progression

27. Dietary restriction
 Protein restriction:
 Reduced intake of animal protein to 0.6–0.8 g/kg/day
 Plant-based diet
 Salt and water restriction
 2g/day of salt
 Volume restriction of 2L in volume overload
 Potassium restriction
 When GFR is ,10-20ml/min/1.7m2, or hyperkalemia
 An aggressive bowel regimen & K+-binding resins
 List of Foods that contain less potassium(50-60mEq/day=2g/d)
 Phosphorous Restriction

28. Medical Management
Drugs eliminated by Kidney to be adjusted or discontinued
 Insulin –hypoglycemia
 Metformin- Lactic acidosis
 Morphine
 Nephrotoxic drugs: NSAIDS, intravenous contrast….
 Magnesium containing laxatives
 Phosphorous containing=g drugs e.g.. cathartics

29. Hypertension & DM
 Target BP 130/80-85 but if DM or proteinuria >1g/day
then 120/80.
Treatment- diuretics, ↓Salt intake, ACE I, ARB,
nondihdropyridines Ca blockers
 Strict Diabetic control
Target bed time glucose 100-140mg/dl, preprandial 80-
120mg/dl
Hb A1c of < 7% additional action if PP>140 or
HbA1c> 8%(ADA guidelines)

30. Treatment of complications
 Hypolipidemic therapy
 Anemia: Target Hb 10-13
– Treatment: EPO, may need iron/folic acid
– Monitor for Fe overload and EPO induced
HTN

31. Treatment of ESKD - RRT
 Early referral to nephrologist in late stage 3 CKD or
rapidly declining GFR
 Team approach; Dietician, Nephorologist…..etc
 Patient education
 Palliative care
 RRT –
 Hemodialysis
 Peritoneal dialysis
 Kidney transplantation

32. Treatment of ESKD - Dialysis
INDICATIONS
 GFR nearing 10ml/min/1.73m2
 Uremic symtpoms
 Fluid overload unresponsive to diuresis
 Refractory hyperkalemia

35. Treatment of ESKD - Hemodialysis
 Vascular access by arterivenous fistula and
prosthetic graft or
 Indwelling catheter
 Complications
 Infections usually staphylococcal species
 Thrombosis
 Aneurysm
 Treatment
 At Centre: 3 times a week @ session lasting 3-5 hours
 At home : More frequently with shorter period

36. Treatment of ESKD - Peritoneal D
 Peritoneal membrane is the dialyzer
 Types : CAPD and CCPD
 Peritonitis frequent complication
 Nausea, vomiting, Abd pain, diarrhea, constipation or fever.
 Normally clear dialysate becomes cloudy
 Diagnostic petinoneal cell count of 100 WBC’s/mcl with differential
of > 50% polymorphonuclear neutrophils
 Staph A most common, but Strep & G-ves may be causative.
 Emepric intraperitoneal Vancomycin or 1st gen Cephalosporins
(cefazolin), + 3rd gen cephalosporin (Ceftazidime), then abx rx later
tailored to culture results

39. Treatment of ESKD - Kidney Trsplnt
 Two-thirds of kidney allografts come from deceased
owners
 The remainder from living related or unrelated donors
 In USA, over 100, 000 on waiting list, average waiting list is
3-7 years depending on geographical location and
receipient blood type

40. Prognosis
 Patients undergoing dialysis have an average 3-5
year life expectancy
 But survival in these patients for as long as 25 years
depends on comorbidities
 Most common cause of death is Cardiac
disease(>50%)
 Other cause include infection, cerebrovascular
disease or malignancy

41. When to refer
 Stage 3-5 CKD should be referred to nephrologist for
management in conjunction with primary care provider.
 Patient with other forms of CKD, such as those with
polycystic kidney disease or proteinuria >1g/day
 Patients with rapidly progressing decline in renal function

42. When to Admit
 Patients with decompensation of CKD
 Worsening acid-base disorder,
 Worsening Electrolyte abnormalities.
 Refractory Volume overload.
 When starting dialysis

43. FURTHER READING………………
 Contents /composition of dialysate used in hemodialysis
and peritoneal dialysis

45. Reference
 Papadakis, M., & Mc Phee, S. J. (2022). Chronic kidney
disease. In Current medical diagnosis and treatment (61
ed., pp. 922-930). USA: Mc Graw Hill.