Chronic kidney disease, Hemodialysis

SHUMAYLA ASLAM, MD
2ND YEAR RESIDENT
EMILIO AGUINALDO COLLEGE MEDICAL
CENTER- CAVITE
DEPARTMENT OF INTERNAL MEDICINE
dr.shumaylaaslam@gmail.com

 CKD is defined as abnormalities of kidney structure or
function, present for<3 months, with implications for
 health.
 Markers of kidney damage
▪ Albuminuria (AER >=30 mg/24 hours; ACR >=30 mg/g [>=3
mg/mmol])
▪ Urine sediment abnormalities
▪ Electrolyte and other abnormalities due to tubular
disorders
▪ Abnormalities detected by histology
▪ Structural abnormalities detected by imaging
▪ History of kidney transplantation
 GFR <60 mL/min/1.73 m2 for > 3 months

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

 History of kidney transplantation.
 Chronic allograft nephropathy (non-specific
findings of tubular atrophy, interstitial fibrosis,
vascular and glomerular sclerosis)
 Rejection
 Drug toxicity (calcineurin inhibitors eg:
tacrolimus, cyclosporin)
 BK virus nephropathy
 Recurrent disease (glomerular disease, oxalosis,
Fabry disease)

1. Diabetic nephropathy
2. Glomerulonephritis
3. Hypertension-associated CKD (includes vascular
and ischemic kidney disease and primary glomerular disease with
associated hypertension)
4. Autosomal dominant polycystic kidney
disease
5. cystic and tubulointerstitial nephropathy

Two broad sets of mechanisms of damage:
1. initiating mechanisms specific to the underlying
etiology
 genetically determined abnormalities in kidney
development or integrity,
 immune complex deposition and inflammation in
certain types of glomerulonephritis,
 toxin exposure in certain diseases of the renal tubules
and interstitium)
2. a set of progressive mechanisms,
 involving hyperfiltration and hypertrophy of the
remaining viable nephrons,
 common consequence following long-term reduction of
renal mass, irrespective of underlying etiology

In the absence of evidence of kidney damage, neither GFR category G1 nor G2 fulfill the criteria
for CKD.

 the pathophysiology of the uremic syndrome
can be divided into manifestations in three
spheres of dysfunction:
1. those consequent to the accumulation of toxins that
normally undergo renal excretion, including
products of protein metabolism;
2. those consequent to the loss of other kidney
functions, such as fluid and electrolyte homeostasis
and hormone regulation; and
3. progressive systemic inflammation and its vascular
and nutritional consequences.

 Hundreds of toxins that accumulate in renal
failure have been implicated in the uremic
syndrome.
 These include water-soluble, hydrophobic,
protein-bound, charged, and uncharged
compounds.
 Nitrogenous excretory products include guanidino
compounds, urates and hippurates, products of
nucleic acid metabolism, polyamines,
myoinositol, phenols, benzoates, and indoles.

 A host of metabolic and endocrine functions
is also impaired or suppressed,
 results in anemia, malnutrition, and abnormal
metabolism of carbohydrates, fats, and proteins.
 plasma levels of many hormones, including PTH,
FGF- 23, insulin, glucagon, steroid hormones
including vitamin D and sex hormones, and
prolactin, change with CKD as a result of reduced
excretion, decreased degradation, or abnormal
regulation.

 CKD is associated with worsening systemic
inflammation.
 Elevated levels of C-reactive protein are detected
along with other acute-phase reactants, decline with
progressive reduction in GFR.
 Thus, the inflammation associated with CKD is
important in the malnutrition-inflammation-
atherosclerosis/calcification syndrome, which
contributes in turn to the acceleration of vascular
disease and comorbidity associated with advanced
kidney disease.

 Earlier stages of CKD (stages 1–3)
 combination of hyperkalemia and hyperchloremic
metabolic acidosis causes non-anion-gap
metabolic acidosis.
 diabetic nephropathy or tubulointerstitial disease
or obstructive uropathy
 Later stages of CKD (stage 4-5)
 anion-gap metabolic acidosis
 Mild: usually corrected with oral sodium
bicarbonate supplementation.
 Modest: protein catabolism;dr.shumaylaaslam@gmail.com

 Treatment:
 Hyponatremia responds to water restriction
 Salt restriction if with evidence of ECFV expansion
 Diuretics +/- metolazone in CKD III-V
 Kaliuretic diuretics for hyperkalemia
 Intractable hyperkalemia is an indication for
dialysis
 Alkali supplementation when HCO3 falls below 20-
23 mmol/L

 Bone manifestations
 High bone turnover with increased PTH levels:
osteitis fibrosa cystica (classic lesion of secondary
hyperparathyroidism)
 Low bone turnover with low or normal PTH levels:
adynamic bone disease and osteomalacia

 PTH
 considered a uremic toxin, and high levels are
associated with muscle weakness, fibrosis of
cardiac muscle, and nonspecific constitutional
symptoms
 Clinical manifestations of severe
hyperparathyroidism include bone pain and
fragility, brown tumors, compression syndromes,
and erythropoietin resistance

 Calciphylaxis (calcific uremic arteriolopathy)
 is a devastating condition
 exclusively in patients with advanced CKD
 patches of ischemic necrosis, especially on the
legs, thighs, abdomen, and breasts
 vascular occlusion in association with extensive
vascular and soft tissue calcification
 Warfarin treatment is considered a risk factor for
calciphylaxis

 Treatment:
 Optimal management is prevention
 Low-phosphate diet
 Use of phosphate-binding agents
▪ calcium acetate and calcium carbonate side effects are
calcium accumulation and hypercalcemia
▪ Sevelamer and lanthanum non-calcium-containing
 Calcitriol suppresses PTH secretion directly

leading cause of morbidity and mortality in CKD patients
 IschemicVascular Disease
 CKD is a major risk factor for ischemic CVD
 Heart Failure
 Abnormal cardiac function from myocardial ischemia, left ventricular
hypertrophy and frank cardiomyopathy
 “low-pressure” pulmonary edema in advanced CKD
 Hypertension and LeftVentricular Hypertrophy
 Hypertension develops early in CKD
 Absence of hypertension may signify a salt-wasting form of CKD,
effect of anti-HPN therapy, volume depletion or poor left ventricular
function
 Use of EPO can also increase BP
 Pericardial Disease
 Chest pain with respiratory accentuation accompanied by friction rub
 Observed in advanced uremia (underdialyzed, non-adherent
patients)

 Treatment:
 In CKD + DM or proteinuria >1 g/day, BP goal is
<130/80 with salt restriction as first-line therapy
 ACEi and ARBs may slow rate of decline of kidney
function but can precipitateAKI and hyperkalemia
 Lifestyle changes
 Management of hyperlipidemia using dietary
measures and statins
 Uremic pericarditis is an absolute indication for urgent
initiation or intensification of dialysis (heparin-free)

 Anemia
 Normocytic, normochromic anemia observed as early as CKD III
and universal in CKD IV
 Causes include:
▪ Relative EPO deficiency
▪ Diminished RBC survival
▪ Bleeding diathesis
▪ Iron deficiency
▪ Hyperparathyroidism/marrow fibrosis
▪ Chronic inflammation
▪ Folate or vitamin B12 deficiency
▪ Hemoglobinopathy
▪ Co-morbids such as hypo/hyperthyroidism, pregnancy, HIV,
autoimmune disease and immunosuppressive drugs
 Current practice is to target a hemoglobin concentration
of 100–115 g/dl

 Abnormal hemostasis
 Prolonged bleeding time, decreased activity of
platelet factor III, abnormal platelet aggregation
and adhesion and impaired prothrombin
consumption
 Greater susceptibility to thromboembolism
especially if with nephrotic-range proteinuria

 Treatment:
 Recombinant human EPO should be initiated once
there are adequate bone marrow iron stores
 Iron supplementation
 Blood transfusions increase the risk of hepatitis, iron
overload, and transplant sensitization; they should be
avoided unless the anemia fails to respond to ESA and
the patient is symptomatic.
 Vitamin B12 and folate supplementation
 Desmopressin, cryoprecipitate, IV conjugated
estrogen and EPO for abnormal bleeding time and
coagulopathy
 Optimal dialysis corrects prolonged bleeding time

 CNS, Peripheral and Autonomic Neuropathy
 Early signs seen at CKD III
 Usually clinically evident at CKD IV
 Management:
 Most resolve with dialysis
 Successful renal transplantation may reverse
residual neurologic changes

 Uremic Fetor:
 urine-like breath odor with dysgeusia (unpleasant
metallic taste)
 Gastritis:
 peptic disease or mucosal ulcerations at any level
of the GI tract
 Anorexia due to retention of uremic toxins
 Protein-Energy Malnutrition (PEM)

 Management:
 Protein restriction may slow the rate of renal
decline at earlier stages
 Daily protein intake 0.60-0.75 g/kg/day with at
least 50% provided by high-biologic value proteins
 0.90 g/kg/day for CKD IV and those with PEM;
daily total caloric intake of 35 kcal/kg
 Calcium and iron supplements may aggravate
constipation and anorexia
 PEM: indication for renal replacement therapy

 Glucose metabolism
 Slowed response to glucose loading
 FBS normal or slightly elevated
 Diminished renal degradation of insulin
 Sexual dysfunction
 Low estrogen, menstrual abnormalities,
inability to carry pregnancies to term
 Reduced plasma testosterone, oligospermia

 Management:
 Goals: FBS 90-130 mg/dL, HbA1Z <7%
 Reduction in insulin and hypoglycemic agent
doses
 Intensive dialysis and successful renal
transplantation may reverse sexual dysfunction

 Pruritus, hyperpigmentation
 Nephrogenic fibrosing dermopathy: progressive
subcutaneous induration especially on the arms and
legs associated with exposure to gadolonium
Treatment:
 Local moisturizers, mild topical steroids, UV radiation
 Minimizing exposure to gadolinium in CKD II and
avoidance in CKD III toV
 Rapid removal of gadolinium by immediate dialysis
for patients in whom MRI is highly necessary

 Renal Ultrasound
 Verifies presence of 2 kidneys, determines symmetry, estimates
size and rules out masses/obstruction
 Finding : bilaterally small kidneys supports CKD (expect for early
DM nephropathy, amyloidosis, HIV nephropathy, polycystic
kidney disease)
 Renal Biopsy
 Not advised for bilaterally small kidneys
 Other contraindications: uncontrolled hypertension, active UTI,
bleeding diathesis (including ongoing anticoagulation) and severe
obesity
 OtherTests
 Perform specific tests to assess for specific target organ
damage

 BP and RAAS interruption
 We recommend that in both diabetic and non-
diabetic adults with CKD and urine albumin
excretion <30 mg/ 24 hours (or equivalent*)
whose office BP is consistently >140mm Hg
systolic or >90mm Hg diastolic be treated with
BP-lowering drugs to maintain a BP that is
consistently </= 140mm Hg systolic and </= 90mm
Hg diastolic.

 We recommend that an ARB or ACE-I be used
in both diabetic and non-diabetic adults with
CKD and urine albumin excretion >300 mg/24
hours (or equivalent*).
 CKD and risk of AKI
 We recommend that all people with CKD are
considered to be at increased risk of AKI.

 Protein intake
 We suggest lowering protein intake to 0.8
g/kg/day in adults with diabetes or without
diabetes and GFR <30 ml/min/ 1.73 m2 (GFR
categories G4-G5), with appropriate education.
 We suggest avoiding high protein intake (>1.3
g/kg/day) in adults with CKD at risk of
progression.

 Glycemic control
 We recommend a target hemoglobin A1c(HbA1c) of
~7.0% (53 mmol/mol) to prevent or delay
progression of the microvascular complications of
diabetes, including diabetic kidney disease. (1A)
 We recommend not treating to an HbA1ctarget of
<7.0% (53 mmol/mol) in patients at risk of
hypoglycemia.

 Salt intake
 We recommend lowering salt intake to <90mmol (<2
g) per day of sodium (corresponding to 5 g of sodium
chloride) in adults, unless contraindicated.
 Lifestyle
 We recommend that people with CKD be encouraged
to undertake physical activity compatible with
cardiovascular health and tolerance (aiming for at
least 30 minutes 5 times per week), achieve a healthy
weight (BMI 20 to 25, according to country specific
demographics), and stop smoking.

 We recommend measuring serum levels of
calcium, phosphate, PTH, and alkaline
phosphatase activity at least once in adults with
GFR <45 ml/min/1.73 m2 (GFR categories G3b-G5)
in order to determine baseline values and inform
prediction equations if used.
 In people with GFR <45 ml/min/1.73 m2 (GFR
categories G3b-G5), we suggest maintaining
serum phosphate concentrations in the normal
range according to local laboratory reference
values.

 We suggest not to routinely prescribe vitamin D
supplements or vitamin D analogs, in the
absence of suspected or documented deficiency,
to suppress elevated PTH concentrations in
people with CKD not on dialysis.
 We suggest that in people with CKD and serum
bicarbonate concentrations <22 mmol/l
treatment with oral bicarbonate
supplementation be given to maintain serum
bicarbonate within the normal range, unless
contraindicated

 We recommend referral to specialist kidney care services for people with CKD
in the following circumstances (1B):
 AKI or abrupt sustained fall in GFR;
 GFR <30 ml/min/1.73 m2 (GFR categories G4-G5)*;
 a consistent finding of significant albuminuria (ACR >=300 mg/g [>=30 mg/mmol]
or AER >=300 mg/
 24 hours, approximately equivalent to PCR >=500 mg/g [>=50 mg/mmol] or PER
>=500 mg/24 hours);
 progression of CKD (see Recommendation 2.1.3 for definition);
 urinary red cell casts, RBC >20 per high power field sustained and not readily
explained;
 CKD and hypertension refractory to treatment with 4 or more antihypertensive
agents;
 persistent abnormalities of serum potassium;
 recurrent or extensive nephrolithiasis;
 hereditary kidney disease.

 We suggest that dialysis be initiated when one
or more of the following are present:
 symptoms or signs attributable to kidney failure
(serositis, acid-base or electrolyte abnormalities,
pruritus);
 inability to control volume status or blood pressure;
 a progressive deterioration in nutritional status
refractory to dietary intervention;
 cognitive impairment.
This often but not invariably occurs in the GFR range
between 5 and 10 ml/min/1.73 m2. (2B)

 Living donor preemptive renal
transplantation in adults should be
considered when the GFR is <20 ml/min/1.73
m2, and there is evidence of progressive and
irreversible CKD over the preceding 6–12
months.

 Absolute indications to start chronic dialysis
include the following:
 Uremic pericarditis or pleuritis.
 Uremic encephalopathy

 Common indications
 Declining nutritional status
 Persistent or difficult to treat volume overload
 Fatigue and malaise
 Mild cognitive impairment
 Refractory acidosis, hyperkalemia, and
hyperphosphatemia

"AEIOU"-
 "A"- intractable acidosis;
 "E"- electrolyte disarray ( K+, Na+, Ca++);
 "I" - intoxicants (methanol ethylene glycol, Li,
ASA);
 "O"- intractable fluid overload;
 "U"- uremic symptoms (nausea, seizure,
pericarditis,bleeding).

 HealthyTransitions Program for chronic kidney disease
(October 2017)
 A randomized trial has shown that an outpatient care
management program utilizing nurse care managers
supported by a protocol-driven informatics system for patients
with late-stage chronic kidney disease (stage 4 to 5 CKD)
decreases hospitalization rates, increases the rate at
which hemodialysis is begun without
a hospitalization, decreases the use of catheters, and increases
the selection of peritoneal dialysis .The informatics system
provided daily reports for each patient that identified
incomplete process steps (including discussions of renal
replacement modality, dietary education, medication
reconciliation, and home safety). Although the trial was small,
these data suggest important benefits of such a program.

Chronic kidney disease, Hemodialysis

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