Topic Outline
• I INTRODUCTION
• II CLINICAL AND LABORATORY MANIFESTATIONS OF CHRONIC KIDNEY DISEASE AND UREMIA
• III EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD
• IV TREATMENT
Topic Outline
I INTRODUCTIONA.PATHOPHYSIOLOGY OF CHRONIC KIDNEY
DISEASEB. IDENTIFICATION OF RISK FACTORS AND
STAGING OF CKDC. ETIOLOGY AND EPIDEMIOLOGYD.PATHOPHYSIOLOGY AND BIOCHEMISTRY OF
UREMIA
Topic OutlineII CLINICAL AND LABORATORY MANIFESTATIONS OF
CHRONIC KIDNEY DISEASE AND UREMIAA. FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS
1. Sodium and water homeostasis2. Potassium homeostasis3. Metabolic acidosis
B. DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM1. Bone manifestations of CKD2. Calcium, phosphorus, and the cardiovascular system3. Other complications of abnormal mineral metabolism
C. CARDIOVASCULAR ABNORMALITIES1. Ischemic vascular disease2. Heart failure3. Hypertension and left ventricular hypertrophy4. Pericardial disease
Topic Outline
II CLINICAL AND LABORATORY MANIFESTATIONS OF CHRONIC KIDNEY DISEASE AND UREMIA
D. HEMATOLOGIC ABNORMALITIES1. Anemia2. Abnormal hemostasis
E. NEUROMUSCULAR ABNORMALITIESF. GASTROINTESTINAL AND NUTRITIONAL ABNORMALITIESG. ENDOCRINE-METABOLIC DISTURBANCESH. DERMATOLOGIC ABNORMALITIES
Topic Outline
III EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD
A.INITIAL APPROACH1.History and physical examination2.Laboratory investigation3.Imaging studies4.Renal biopsy
B.ESTABLISHING THE DIAGNOSIS AND ETIOLOGY OF CKD
Topic OutlineIV TREATMENTA.SLOWING THE PROGRESSION OF CKD
1.Reducing Intraglomerular Hypertension and ProteinuriaB.SLOWING PROGRESSION OF DIABETIC RENAL DISEASE
1.Control of Blood Glucose2.Control of Blood Pressure and Proteinuria3.Protein Restriction
C.MANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE1.Medication Dose Adjustment2.Preparation for Renal Replacement Therapy3.Patient Education
Abbreviations• NKF - National Kidney Foundation
• KDOQI - Kidney Disease Outcomes Quality Initiative
• KDIGO - Kidney Disease Improving Global Outcomes
What is CKD?• CKD is defined by the
– presence of kidney damage or decreased kidney function
– for three or more months, – irrespective of the cause.
What is CKD?• The persistence of the damage or decreased
function for at least three months is necessary to distinguish CKD from acute kidney disease.
• Kidney damage refers to pathologic abnormalities, whether established via:1. renal biopsy or 2. imaging studies, or 3. inferred from markers such as
a) urinary sediment abnormalities or b) increased rates of urinary albumin
excretion.
What is CKD?• Chronic kidney disease is defined based on
the presence of either kidney damage or decreased kidney function for three or more months, irrespective of cause.
• Criteria:Duration ≥3 months, based on documentation
or inferenceGlomerular filtration rate (GFR) <60
mL/min/1.73 m2Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
CHRONIC KIDNEY DISEASE Duration ≥3 months, based on
documentation or inference
Duration is necessary to distinguish chronic from acute kidney diseases.
1. Clinical evaluation can often suggest duration2. Documentation of duration is usually not
available in epidemiologic studies
CHRONIC KIDNEY DISEASE
GFR is the best overall index of kidney function in health and disease.1. The normal GFR in young adults is approximately
125 mL/min/1.73 m2; GFR <15 mL/min/1.73 m2 is defined as kidney failure
2. Decreased GFR can be detected by current estimating equations for GFR based on serum creatinine (estimated GFR) but not by serum creatinine alone
3. Decreased estimated GFR can be confirmed by measured GFR
Glomerular filtration rate (GFR) <60 mL/min/1.73 m2
CHRONIC KIDNEY DISEASE
A) Pathologic abnormalities (examples). Cause is based on underlying illness and pathology. Markers of kidney damage may reflect pathology.
1. Glomerular diseases (diabetes, autoimmune diseases, systemic infections, drugs, neoplasia)
2. Vascular diseases (atherosclerosis, hypertension, ischemia, vasculitis, thrombotic microangiopathy)
3. Tubulointerstitial diseases (urinary tract infections, stones, obstruction, drug toxicity)
4. Cystic disease (polycystic kidney disease)
Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
CHRONIC KIDNEY DISEASE
B) History of kidney transplantation. In addition to pathologic abnormalities observed in native kidneys, common pathologic abnormalities include the following:
1. Chronic allograft nephropathy (non-specific findings of tubular atrophy, interstitial fibrosis, vascular and glomerular sclerosis)
2. Rejection3. Drug toxicity (calcineurin inhibitors)4. BK virus nephropathy5. Recurrent disease (glomerular disease, oxalosis, Fabry
disease)
Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
CHRONIC KIDNEY DISEASE
C) Albuminuria as a marker of kidney damage (increased glomerular permeability, urine albumin-to-creatinine ratio [ACR] >30 mg/g).*
1. The normal urine ACR in young adults is <10 mg/g. Urine ACR categories 10-29, 30-300 and >300 mg are termed "high normal, high, and very high" respectively. Urine ACR >2200 mg/g is accompanied by signs and symptoms of nephrotic syndrome
2. Threshold value corresponds approximately to urine dipstick values of trace or 1+
3. High urine ACR can be confirmed by urine albumin excretion in a timed urine collection
Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
CHRONIC KIDNEY DISEASE
D) Urinary sediment abnormalities as markers of kidney damage
1. RBC casts in proliferative glomerulonephritis2. WBC casts in pyelonephritis or interstitial nephritis3. Oval fat bodies or fatty casts in diseases with
proteinuria4. Granular casts and renal tubular epithelial cells
in many parenchymal diseases (non-specific)
Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
CHRONIC KIDNEY DISEASE
E) Imaging abnormalities as markers of kidney damage (ultrasound, computed tomography and magnetic resonance imaging with or without contrast, isotope scans, angiography).
1. Polycystic kidneys2. Hydronephrosis due to obstruction3. Cortical scarring due to infarcts, pyelonephritis or
vesicoureteral reflux4. Renal masses or enlarged kidneys due to infiltrative
diseases5. Renal artery stenosis6. Small and echogenic kidneys (common in later stages
of CKD due to many parenchymal diseases)
Kidney damage, as defined by structural abnormalities or functional abnormalities other than decreased GFR
PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASETwo broad sets of mechanismsof damage:
1. initiating mechanisms specific to the underlying etiology
2. a set of progressive mechanisms- hyperfiltration and hypertrophy of the remaining viable nephrons
PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASETwo broad sets of mechanismsof damage:
1. initiating mechanisms specific to the underlying etiology
2. a set of progressive mechanisms- hyperfiltration and hypertrophy of the remaining viable nephrons
PATHOPHYSIOLOGY OF CHRONIC KIDNEY DISEASEIncreased intrarenal activity of the renin-angiotensin axis appears to contribute both to:
initial adaptive hyperfiltration the subsequent maladaptive
hypertrophy and sclerosis (TGF-β)
Left: Schema of the normal glomerular architecture.Right: Secondary glomerular changes
IDENTIFICATION OF RISK FACTORS AND STAGING OF CKDRisk factors:
1. hypertension, 2. diabetes mellitus, 3. autoimmune disease, 4. older age, 5. African ancestry, 6. a family history of renal disease, 7. a previous episode of acute kidney injury, 8. and the presence of
a. proteinuria, b. abnormal urinary sediment, or c. structural abnormalities of the urinary tract
Recommended Equations for Estimation of Glomerular Filtration Rate (GFR) Using Serum Creatinine Concentration (PCr), Age, Sex, Race, and Body Weight
1) Equation from the Modification of Diet in Renal Disease study∗ (MDRD)
2) Cockcroft-Gault equation
CKD
IDENTIFICATION OF RISK FACTORS AND STAGING OF CKD
Chronic renal damagePersistence in the urine of:
>17 mg of albumin per gram of creatinine in adult males and
25 mg albumin per gram of creatinine in adult females
ETIOLOGY AND EPIDEMIOLOGYLeading Categories of Etiologies
of CKD∗ Diabetic glomerular disease Glomerulonephritis
Hypertensive nephropathy Primary glomerulopathy with
hypertension Vascular and ischemic renal disease Autosomal dominant polycystic kidney
disease Other cystic and tubulointerstitial
nephropathy
ETIOLOGY AND EPIDEMIOLOGYNewly diagnosed CKD:
present with hypertension
CKD is often attributed to hypertension:When no overt evidence for a primary
glomerular or tubulointerstitial kidney disease process is present
ETIOLOGY AND EPIDEMIOLOGY
Two Categories:1) patients with a silent
primary glomerulopathy2) patients in whom
progressive nephrosclerosis and hypertension is the renal correlate of a systemic vascular disease
Multiple Functions of the Kidneys1) Excretion of metabolic waste products and foreign chemicals2) Regulation of water and electrolyte balances3) Regulation of body fluid osmolality and electrolyte concentrations
4) Regulation of arterial pressure
5) Regulation of acid-base balance
6) Secretion, metabolism, and excretion of hormones
7) Gluconeogenesis
PATHOPHYSIOLOGY AND BIOCHEMISTRY OF UREMIAElevated waste products:
Hundreds of toxins, water-soluble, hydrophobic, protein- bound, charged, and uncharged compounds, guanidinocompounds, urates and hippurates, products of nucleic acid metabolism, polyamines, myoinositol, phenols, benzoates,and indoles
‘middle molecules’
PATHOPHYSIOLOGY AND BIOCHEMISTRY OF UREMIAA host of metabolic and endocrine functions normally performed by the kidneys is also impaired or suppressed:
anemia, malnutrition, and abnormal metabolism of
carbohydrates, fats, and proteins
PATHOPHYSIOLOGY AND BIOCHEMISTRY OF UREMIAUrinary retention, decreased degradation, or abnormal regulation of hormones
PTH, FGF-23, insulin, glucagon, steroid hormones including vitamin D and sex hormones, andprolactin
3 Spheres of dysfunction of Uremic Syndrome
Toxins
HomeostasisProgressive
systemic inflammation
UREM
CLINICAL AND LABORATORY MANIFESTATIONS OFCHRONIC KIDNEY DISEASE AND UREMIA
CLINICAL ABNORMALITIES IN UREMIA1. Fluid and electrolyte disturbances2. Endocrine-metabolic disturbances3. Neuromuscular disturbances4. Cardiovascular and pulmonary
disturbances5. Dermatologic disturbances6. Gastrointestinal disturbances7. Hematologic and immunologic disturbances
(I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
CLINICAL ABNORMALITIES IN UREMIA1. Fluid and electrolyte disturbances
a. Volume expansion (I)b. Hyponatremia (I)c. Hyperkalemia (I)d. Hyperphosphatemia (I)
(I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
CLINICAL ABNORMALITIES IN UREMIA
1. Secondary hyperparathyroidism (I or P)
2.Adynamic bone (D)3. Vitamin D–deficient
osteomalacia (I)4. Carbohydrate resistance
(I)5. Hyperuricemia (I or P)6. Hypertriglyceridemia (I or
P)7. Increased Lp(a) level (P)
8. Decreased high-density lipoprotein level (P)
9. Protein-energy malnutrition (I or P)
10.Impaired growth and development (P)
11.Infertility and sexual dysfunction (P)
12.Amenorrhea (I/P)13.β2-Microglobulin–
associated amyloidosis (P or D)(I) improves with an optimal program of dialysis and
related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
2. Endocrine-metabolic disturbances
CLINICAL ABNORMALITIES IN UREMIA
1.Fatigue (I)b2.Sleep disorders (P)3.Headache (P)4.Impaired mentation (I)b5.Lethargy (I)b6.Asterixis (I)7.Muscular irritability8.Peripheral neuropathy (I
or P)9.Restless legs syndrome
(I or P)
10.Myoclonus (I)11.Seizures (I or P)12.Coma (I)13.Muscle cramps (P or D)14.Dialysis
disequilibrium syndrome (D)
15.Myopathy (P or D)
(I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
3. Neuromuscular disturbances
CLINICAL ABNORMALITIES IN UREMIA
1.Arterial hypertension (I or P)
2.Congestive heart failure or pulmonary edema (I)
3.Pericarditis (I)4.Hypertrophic or dilated
cardiomyopathy (I, P, or D)
5.Uremic lung (I)6.Accelerated
atherosclerosis (P or D)7.Hypotension and
arrhythmias (D)8.Vascular calcification
(P or D)
(I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
4. Cardiovascular and pulmonary disturbances
CLINICAL ABNORMALITIES IN UREMIA
1.Pallor (I)b2.Hyperpigmentation (I, P, or D)3.Pruritus (P)4.Ecchymoses (I)5.Nephrogenic fibrosing dermopathy (D)6.Uremic frost (I)
(I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
5. Dermatologic disturbances
CLINICAL ABNORMALITIES IN UREMIA
1.Anorexia (I)2.Nausea and vomiting (I)3.Gastroenteritis (I)4.Peptic ulcer (I or P)5.Gastrointestinal bleeding (I, P, or D)6.Idiopathic ascites (D)7.Peritonitis (D)
(I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
6. Gastrointestinal disturbances
CLINICAL ABNORMALITIES IN UREMIA
1.Anemia (I)b2.Lymphocytopenia (P)3.Bleeding diathesis (I or D)b4.Increased susceptibility to infection5.(I or P)6.Leukopenia (D)7.Thrombocytopenia (D)
(I) improves with an optimal program of dialysis and related therapy; (P) persist or even progress, despite an optimal program; (D) develops only after initiation of dialysis therapy.
7. Hematologic and immunologic disturbances
FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS
SODIUM
FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS
Hyponatremia – water restriction
ECFV expansion – salt restriction
Thiazides – limited utility in stages 3-5 CKD- loop diuretics needed
Loop Diuretics resistance – Higher doses
Metolazone – combined with loop diuretics, which inhibits the sodium chloride co-transporter of the distal convoluted tubule, can help effect renal salt excretion
SODIUM
FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS
• HYPERKALEMIA• Precipitated by• increased dietary potassium intake, • protein catabolism, • hemolysis, • hemorrhage, • transfusion of stored red blood cells, • and metabolic acidosis• Medications
POTASSIUM
Renal Potassium
Handling
FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS
Hypokalemia:• Not common in CKD• reduced dietary potassium intake• GI losses• Diuretic therapy• Fanconi’s syndrome• RTA• Hereditary or acquired Tubulointerstitial
disease
POTASSIUM
FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS
Metabolic acidosis• common disturbance in advanced CKD• combination of hyperkalemia and
hyperchloremic metabolic acidosis is often present, even at earlier stages of CKD (stages 1–3)
• Treat hyperkalemia• the pH is rarely <7.35• usually be corrected with oral sodium
bicarbonate supplementation
MET ACIDOSIS
FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS
Renal Control of Acid-Base Balance1) Secretion of H+ and Reabsorption of HCO3 by the
Renal Tubulesa. H+ is Secreted by Secondary Active Transport in the Early
Tubular Segmentsb. Filtered HCO3 is Reabsorbed by Interaction with H+ in the
Tubulesc. Primary Active Secretion of H+ in the Intercalated Cells
of Late Distal and Collecting Tubules2) Combination of Excess H+ with Phosphate and
Ammonia Buffers in the Tubule Generates “New” HCO3a. Phosphate Buffer System Carries Excess H+ into the Urine
and Generates New HCO3 b. Excretion of Excess H+ and Generation of New HCO3 by
the Ammonia Buffer System
MET ACIDOSIS
Renal Handling of Acid
Excretion
• To maintain euvolemia:• Adjustments in the dietary intake of salt • and use of loop diuretics, occasionally in combination
with metolazone• Hyponatremia:
• water restriction• Hyperkalemia
• responds to dietary restriction of potassium, • avoidance of potassium supplements • use of kaliuretic diuretics• potassium-binding resins, such as calcium resonium or
sodium polystyrene• The renal tubular acidosis and subsequent
anion-gap metabolic acidosis• alkali supplementation, typically
with sodium bicarbonate
DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM
The principal complications of abnormalities of calcium and phosphate metabolism in CKD
1. occur in the skeleton and 2. the vascular bed, 3. with occasional severe involvement of
extraosseous soft tissues
Bone manifestations of CKD, classified as:• associated with high bone turnover with
increased PTH levels• low bone turnover with low or normal PTH
levels
DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM
The pathophysiology of secondary hyperparathyroidism:
1. Declining GFR leads to reduced excretion of phosphate
2. increased synthesis of PTH and growth of parathyroid gland mass
3. decreased levels of ionized calcium, resulting from diminished calcitriol production by the failing kidney
Fibroblast growth factor 23 (FGF-23) (1) increased renal phosphate excretion;
(2) stimulation of PTH, which also increases renal phosphate excretion; and
(3) suppression of the formation of 1,25(OH)2D3, leading to diminished phosphorus absorption from the gastrointestinal tract
DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM
Osteitis fibrosa cystica bone turnover abnormal histology brown tumor
Low-turnover bone disease can be grouped into two categories:
1. adynamic bone disease 2. and osteomalacia
DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM
Calcium, phosphorus, and the cardiovascular system:
• Hyperphosphatemia and hypercalcemia are associated with increased vascular calcification
• calcification of the media in coronary arteries and even heart valves
• ingested calcium cannot be deposited in bones with low turnover
• osteoporosis and vascular calcification • hyperphosphatemia can induce a change
in gene expression in vascular cells
DISORDERS OF CALCIUM AND PHOSPHATE METABOLISM
Other complications of abnormal mineral metabolism:
• Calciphylaxis (calcific uremic arteriolopathy)
• Other etiologies• use of oral calcium as a
phosphate binder• Warfarin
Sevelamer and lanthanum – non calcium containing polymersCalcitriol exerts a direct suppressive effect on PTH secretion and also indirectly suppresses PTH secretion by raising the concentration of ionized calcium
recommended target PTH level between 150 and 300 pg/mL
CARDIOVASCULAR ABNORMALITIES1) Ischemic vascular disease
The CKD-related risk factors comprise 1. anemia, 2. hyperphosphatemia,3. hyperparathyroidism, 4. sleep apnea, and 5. generalized inflammation
Cardiac troponin levels are frequently elevated in CKD without evidence of acute ischemia.
CARDIOVASCULAR ABNORMALITIES2) Heart failure
“bat wing” distribution - form of “low-pressure” pulmonary edema
CARDIOVASCULAR ABNORMALITIES3) Hypertension and left ventricular hypertrophy• anemia and the placement of an
arteriovenous fistula• low blood pressure actually carries
a worse prognosis than does high blood pressure
• erythropoiesis-stimulating agents
MANAGEMENT OF HYPERTENSION• Blood pressure should be reduced
to 125/75• Salt restriction should be the first
line of therapyMANAGEMENT OF CARDIOVASCULAR DISEASE• Lifestyle changes, including
regular exercise• Manage dyslipidemia
Pericardial diseaseChest pain with respiratory accentuation, accompanied by a friction rub, is diagnostic of pericarditis.
Classic electrocardiographic abnormalities include PR-interval depression and diffuse ST-segment elevation
Initiation of dialysis No heparin
HEMATOLOGIC ABNORMALITIESAnemia
A normocytic, normochromic anemia is observed as early as stage 3 CKD and is almost universal by stage 4.
The primary cause in patients with CKD is insufficient production of erythropoietin (EPO) by the diseased kidneys.
Causes of Anemia in CKD1. Relative deficiency of erythropoietin2. Diminished red blood cell survival3. Bleeding diathesis4. Iron deficiency5. Hyperparathyroidism/bone marrow fibrosis6. “Chronic inflammation”7. Folate or vitamin B12 deficiency8. Hemoglobinopathy9. Comorbid conditions: hypo/hyperthyroidism,
pregnancy, HIV-associated disease, autoimmune disease, immunosuppressive drugs
recombinant human EPO and modified EPOProducts
Use of EPO in CKD may be associated with an:1. increased risk of stroke in those with type 2
diabetes, 2. an increase in thromboembolic events, 3. and perhaps a faster progression to the need
for dialysistarget a hemoglobin concentration of 100–115 g/L
HEMATOLOGIC ABNORMALITIESAbnormal hemostasis
1. prolonged bleeding time, 2. decreased activity of platelet factor III, 3. abnormal platelet aggregation and
adhesiveness, 4. and impaired prothrombin consumption.
Clinical manifestations include 5. an increased tendency to bleeding and
bruising,6. prolonged bleeding from surgical incisions,7. menorrhagia,8. and spontaneous GI bleeding
Abnormal bleeding time and coagulopathy in patients with renal failure may be reversed temporarily with
• desmopressin(DDAVP), • cryoprecipitate, • IV conjugated estrogens, • blood transfusions, and • EPO therapy.
Optimal dialysis will usually correct a prolonged bleeding time.
NEUROMUSCULAR ABNORMALITIESCentral nervous system (CNS), peripheral, and autonomic neuropathy
mild disturbances in memory and concentration and sleep disturbance.
Neuromuscular irritability, including hiccups, cramps,and fasciculations or twitching of muscles, becomes evident at later stages.
In advanced untreated kidney failure, asterixis, myoclonus,seizures, and coma can be seen
GASTROINTESTINAL AND NUTRITIONAL ABNORMALITIES
Uremic fetor , a urine-like odor on the breath, derives from the breakdown of urea to ammonia in saliva and is often associated with an unpleasant metallic taste (dysgeusia)
DERMATOLOGIC ABNORMALITIESPruritus
nephrogenicfibrosing dermopathy
EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD
Laboratory investigation
Serial measurements of renal function
Serum concentrations of calcium, phosphorus, vitamin D, and PTH should be measured to evaluatemetabolic bone disease.
Hemoglobin concentration, iron, B 12 , andFolate
A 24-h urine collection
EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD
Imaging studies
most useful imaging study is a renal ultrasoundCKD with normal sized kidneys
DM nephropathyamyloidosisHIV nephropathy
voiding cystogramjudicious administration of sodium bicarbonate-containing solutions and N -acetyl-cysteine
ESTABLISHING THE DIAGNOSIS AND ETIOLOGY OF CKD
Renal biopsyContraindications:
• bilaterally small kidneys• uncontrolled hypertension, • active urinary tract infection,• bleeding diathesis (including ongoing
anticoagulation), • and severe obesity
EVALUATION AND MANAGEMENT OF PATIENTS WITH CKD
The most important initial diagnostic step in the evaluation of a patient presenting with elevated serum creatinine is to distinguish newly diagnosed CKD from acute or subacute renal failure
SUGGESTS CHRONICITY1. hyperphosphatemia,2. hypocalcemia, 3. elevated PTH and bone alkaline
Phosphatase4. Normochromic, normocytic anemia5. bilaterally reduced kidney size
<8.5 cm
Topic OutlineIV TREATMENTA.SLOWING THE PROGRESSION OF CKD
1.Reducing Intraglomerular Hypertension and Proteinuria
B.SLOWING PROGRESSION OF DIABETIC RENAL DISEASE1.Control of Blood Glucose2.Control of Blood Pressure and Proteinuria3.Protein Restriction
C.MANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE1.Medication Dose Adjustment2.Preparation for Renal Replacement Therapy3.Patient Education
TREATMENT
TREATMENTAny acceleration in the rate of decline should prompt a search for superimposed acute or subacute processes that may be reversible1. ECFV depletion, 2. uncontrolled hypertension, 3. urinary tract infection, 4. new obstructive uropathy, 5. exposure to nephrotoxic agents6. and reactivation or flare of the original7. disease, such as lupus or vasculitis
TREATMENTSLOWING THE PROGRESSION OF CKD:Reducing Intraglomerular Hypertension and Proteinuria
renoprotective effect of antihypertensive medications - ↓proteinuria125/75 mmHg as the target blood pressure ACE inhibitors and ARBsAdverse effects from these agents include cough and angioedema with ACE inhibitors, anaphylaxis, and hyperkalemia with either class2nd line - diltiazem and verapamil
TREATMENTSLOWING PROGRESSION OF DIABETIC RENAL DISEASEControl of Blood Glucose
preprandial glucose be kept in the 5.0–7.2 mmol/L, (90–130 mg/dL)hemoglobin A 1C should be < 7% use and dose of oral hypoglycemic needs to be reevaluated
ChlorpropramideMetforminThiazolidinediones
TREATMENTSLOWING PROGRESSION OF DIABETIC RENAL DISEASEControl of Blood Pressure and Proteinuria
albuminuriaa strong predictor of cardiovascular events and nephropathy
Microalbumin testingAt least ANNUALLY
TREATMENTSLOWING PROGRESSION OF DIABETIC RENAL DISEASEProtein Restriction
CKD – 0.60 and 0.75 g/kg per dayat least 50% of the protein intake be of high biologic valueStage 5 CKD - 0.9g/kg/dayCaloric requirement – 35cal/kg/day
TREATMENTMANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE1. Medication Dose Adjustment
loading dose – no dose adjustment>70% excretion is by a nonrenal route
– no adjustmentNSAIDs should be avoidedNephrotoxic medical imaging radiocontrast agents and gadolinium should be avoidedhttp://www.globalrph.com/renaldosing2.htm
TREATMENTMANAGING OTHER COMPLICATIONS OF CHRONIC KIDNEY DISEASE1. Medication Dose Adjustment2. Preparation for Renal Replacement
Therapy
symptoms and signs of impending uremia, such as anorexia, nausea, vomiting, lassitude – RX with Protein restrictionoptimal time for initiation of renal replacement therapy have been established – KDOQIDelaying – worse prognosis
HEMODIALYSIS
ABSOLUTE INDICATIONS:●Uremic pericarditis or pleuritis●Uremic encephalopathy
Common indications:1. Declining nutritional status2. Persistent or difficult to treat volume
overload3. Fatigue and malaise4. Mild cognitive impairment5. Refractory acidosis, hyperkalemia, and
hyperphosphatemia
Chronic Kidney Disease
Leading Categories of Etiologiesof CKD∗
Renal Potassium
Handling
Normal Lab Values
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