CHRONIC KIDNEY DISEASE

Presenter: Dr Yusra Javed

DEFINITION
• CKD is an irreversible deterioration in kidney
function that usually develops in a period of
years.
• Structural or functional abnormalities of the
kidney for ≥3 months manifested by kidney
damage, with or without decreased GFR.
OR
• GFR <60mL/min/1.73m², with or without
kidney damage.
CLASSIFICATION

CKD is classified according to:

• Glomerular Filtration Rate
• Albuminuria
EPIDEMIOLOGY
• Prevalence of CKD stages
3–5 are around 5%–7%.
• Mostly affects people aged
65 years and above.
• Prevalence in patients with
HTN, diabetes and vascular
disease is higher.
• More than 25% of the
population aged over 75
have an eGFR of <60
mL/min/1.73m².
CAUSES
PATHOPHYSIOLOGY
• Electrolyte Abnormalities: Hyperkalemia, hyperphosphatemia, hypocalcemia,
hypermagnesemia
• Water Imbalance: Decreased GFR → Decreased water filtration → Increased
water retention
• Uremia: Failure of removal of waste products → Buildup of urea → Tissue and
organ damage
• Hormone Imbalances: Decreased EPO → Decreased RBC production.
Decreased GFR → Activation of Renin-Angiotensin-Aldosterone system →
Increased vasoconstriction. Secondary hyperparathyroidism
• Metabolic Acidosis: Damaged kidneys unable to excrete H+ and reabsorb
Bicarbonate.
• Albumin Regulation: Hypoalbuminemia → Decreased oncotic pressure →
Fluid overload. Liver responds by producing more lipoproteins (triglycerides,
LDL) → Hyperlipidemia
 CLINICAL FEATURES
• Most patients asymptomatic until GFR <30
mL/min/1.73m²
• Raised Urea and creatinine found incidentally during
routine blood tests of high risk patients.
• Clinical manifestations depend upon severity and
progression of disease as well as the systems
involved.
1. Cardiovascular
a. HTN
• Secondary to salt and water retention—decreased GFR stimulates
renin–angiotensin system and aldosterone secretion to increase,
which leads to an increase in BP.
• Renal failure is the most common cause of secondary HTN.
b. CHF—due to volume overload, HTN, and anemia.
c. Pericarditis (uremic).

2. Gastrointestinal (usually due to uremia).

a. Nausea, vomiting.
b. Loss of appetite (anorexia).
3. Neurologic
a. Symptoms include lethargy, somnolence, confusion, peripheral
neuropathy, and uremic seizures. Physical findings include weakness,
asterixis, and hyperreflexia.
b. Hypocalcemia can cause lethargy, confusion, and tetany.

4. Hematologic
a. Normocytic normochromic anemia (secondary to deficiency of
erythropoietin)—may be severe.
b. Bleeding secondary to platelet dysfunction (due to uremia). Platelets
do not degranulate in uremic environment.
5. Endocrine/metabolic
a. Calcium–phosphorus disturbances.
• Decreased renal clearance of phosphate leads to hyperphosphatemia. This
leads to hypocalcemia, which causes secondary hyperparathyroidism.
• Secondary hyperparathyroidism causes renal osteodystrophy, which causes
weakening of bones and possibly fractures.
• Hyperphosphatemia may cause calcium and phosphate to precipitate, which
causes vascular calcifications that may result in necrotic skin lesions. This is
called calciphylaxis and is usually irreversible.
b. Sexual/reproductive symptoms due to hypothalamic–pituitary disturbances
and gonadal response to sex hormones: in men, decreased testosterone; in
women, amenorrhea, infertility, and hyperprolactinemia.
c. Pruritus (multifactorial etiology)—common and difficult to treat.
6. Fluid and electrolyte problems.
a. Volume overload—watch for pulmonary edema.
b. Hyperkalemia—due to decreased urinary secretion.
c. Hypermagnesemia—occurs secondary to reduced urinary loss.
d. Hyperphosphatemia
e. Metabolic acidosis—due to loss of renal mass (and thus decreased production of
ammonia, which the kidneys use to buffer excreted acid) and the kidney’s inability
to excrete H+ itself.

7. Immunologic—uremia inhibits cellular and humoral immunity, leading to

increased susceptibility to infections.
 INVESTIGATIONS
Main aim is to:
• Exclude AKI: in patients with unexpectedly high urea and
creatinine, renal function should be retested within 2 weeks to
avoid missing AKI.
• Identify the underlying cause where possible.
• Identify reversible factors, such as HTN or urinary tract
obstruction
• Screen for complications, such as anemia and renal
osteodystrophy
• Screen for cardiovascular risk factors.
 MANAGEMENT

The aims of management in CKD are to:

• monitor renal function
• prevent or slow further renal damage
• limit complications of renal failure
• treat risk factors for cardiovascular disease
• prepare for RRT, if appropriate
 MONITORING
RENAL FUNCTION
• Renal function should be
monitored every 6 months
in patients with stage 3
CKD, but more frequently
in patients who are
deteriorating rapidly or
have stage 4 or 5 CKD.
• A plot of GFR against time
can demonstrate whether
therapy has been
successful in slowing
 REDUCING RATE OF PROGRESSION
• Treat the primary cause
• Tight blood pressure control is applicable to CKD
regardless of cause.
• Reducing proteinuria in those with glomerular
disease.
Antihypertensive Therapy
• Lowering of blood pressure slows the rate at which renal function declines in CKD, lowering
the risk of hypertensive heart failure and cardiovascular disease.
• A target blood pressure of less than 140/90 mmHg is recommended for patients with CKD
and no albuminuria (ACR < 3mg/mmol).
• A lower target of 130/80 mmHg is recommended for those with moderately elevated
albuminuria (ACR 3-30mg/mmol).
• 125/75m mmHg for patients with heavy proteinuria (ACR > 70mg/mmol)
• ACE inhibitors (lisinopril, captopril) are preferred, but multiple drugs including diuretics may
be used.
Reduction of Proteinuria
• ACE inhibitors or ARBs (valsartan, losartan) should be prescribed to all
patients with diabetic nephropathy and patients with CKD and
proteinuria, irrespective of whether hypertension is present.
• Taken with caution as it may exacerbate pre-renal failure (should not be
given in patients with baseline potassium >5.5mmol/L).
• Glycemic control (if patient is diabetic) prevents worsening or
proteinuria.
 TREATING
• Maintenance of fluid and electrolyte balance
COMPLICATIONS
i. Urea ↑: prevent excessive consumption of protein.
ii. Hyperkalemia: daily potassium intake <70 mmol, Potassium-binding compounds (patiromer),
reduce drugs that elevate potassium.
iii. Volume expansion: low-sodium diet (<100 mmol/24 hrs), Diuretics(loop
diuretics/combinations of loop, thiazide & potassium-sparing diuretics)
• Acid-Base balance: Metabolic acidosis corrected with sodium bicarbonate supplements.
• Anemia: Iron supplements, recombinant human erythropoietin, (avoidance of blood
transfusions as it may cause hypertension/ thrombosis)
• Renal Bone Disease: Hyperphosphatemia treated by dietary restriction (milk, cheese, eggs,
protein-rich foods) and by phosphate-binding drugs that inhibit phosphate reabsorption in
the gut (calcium carbonate, aluminum hydroxide, sevelamer).
• Bleeding: Desmopressin; Pruritis: UV light; Endocrinopathy: Estrogen and Testosterone
replacement.
 TREATING RISK FACTORS FOR
CARDIOVASCULAR DISEASE
• Healthy lifestyle, regular exercise, weight loss and smoking cessation
• Lipid-lowering drugs (statins)
• Low protein—to 0.7 to 0.8 g/kg body weight per day: data suggests this may slow
progression of CKD.
• Use a low-salt diet if HTN, CHF, or oliguria are present.
• Restrict potassium, phosphate, and magnesium intake.
PREPARING FOR RENAL REPLACEMENT THERAPY
• Timely referral to a nephrologist
• Commence RRT when symptoms of CKD begin to impact on quality of life but
before serious complications occur.
• Preparations for starting RRT at least 12 months before the predicted start
date (psychological and social support, assessing home circumstances,
discussing choices of treatment).
• Physical preparations include timely access for dialysis and Hepatitis B
vaccination.
• Renal Transplantation is the only definitive cure, RRT is just a bridge to it.
THANK YOU