Nephrorounds3 2015final-150907110921-lva1-app6892

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


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


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)



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



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)



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)


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)


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


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)


3. Neuromuscular disturbances


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)


4. Cardiovascular and pulmonary disturbances


1.Pallor (I)b2.Hyperpigmentation (I, P, or D)3.Pruritus (P)4.Ecchymoses (I)5.Nephrogenic fibrosing dermopathy (D)6.Uremic frost (I)


5. Dermatologic disturbances


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)


6. Gastrointestinal disturbances


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)


7. Hematologic and immunologic disturbances

FLUID, ELECTROLYTE, AND ACID-BASE DISORDERS

SODIUM


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


• 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


Hypokalemia:• Not common in CKD• reduced dietary potassium intake• GI losses• Diuretic therapy• Fanconi’s syndrome• RTA• Hereditary or acquired Tubulointerstitial

disease

POTASSIUM


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


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


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


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


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


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


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


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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