case presentation, and case discussion

1. CHRONIC KIDNEY
DISEASE
(CKD)

2. CASE PRESENTATION:
HISTORY:
24Y old female presented to us with history of
shortness of breath which was gradual in onset,
progressive, worsened on lying flat associated
with facial puffiness and pedal edema. there is
also history of vomiting after eating something.
PAST HISTORY:
Diagnosed with DM at age 13
Has not been compliant with prescribed
treatment.

3. GENERAL PHYSICAL
EXAMINATION:
 Edema
 In extremities, face, and eyes
 Shortness of breath
 pallor
VITALS:
Pulse: 92/min
BP: 140/90
RR: 28/Min
TEMP: afebrile

4. SYSTEMIC EXAMINATION:
 CNS: GCS 15/15
 CVS: S1 + S2+ 0
 RS: NVB+ Bilateral crepts at bases
 GIT: Abd distended soft non tender, no
visceromegaly

5. INVESTIGATION:
 CBC:
HB: 7.8mg/dl
WBC: 8900
MCV: 92
PLATELET: 140000
 UREA: 67
 CREATININE: 10
 Na: 145
 K: 5.6

6.  USG ABDOMEN AND KUB:
Kidney size are smaller, and reduced CMD and
increased echogenicity
moderate abdominopelvic ascites

7. TREATMENT GIVEN:
 IV Lasix 40mg TDS
 IV Nephrosteril OD
 IV Soda bicarb 30cc TDS
 INJ Erythropoietin 4000 IU SC Weekly
 BSR TDS
 InJ INSULIN R Acc to S/S
 HD Twice weekly

8. Nutrition Intervention
 Goal 1
 Lower serum potassium to normal range
 Limit dietary potassium to 2 g/day
 Educate on implications on health if excess
potassium is consumed
 Educate on foods both high and low in potassium

9. Nutrition Intervention
 Goal 2
 Reduce fluid retention gains to acceptable
range per dialysis treatment
 Limit dietary sodium to 2 g/day
 Educate on implications on health of consuming
excess sodium and fluid intake
 Educate on foods both high and low in sodium
and in fluids.

10. Chronic Kidney Disease:
 Kidney damage or a decrease in kidney
function that lasts over three month
 Kidney function measured by the glomerular
filtration rate (GFR)
 A GFR less than 60 cc/min/1.73 m2 for more
than 3 months indicates CKD
 5 stages of disease; GFR indicates which
stage a patient is in

11. Diagnostic Measures
 Stage 1: GFR > 90 mL/min/1.73 m²
 Normal or elevated GFR
 Stage 2: GFR 60-89 (mild)
 Stage 3: GFR 30-59 (moderate)
 Stage 4: GFR 15-29 (severe)
 Stage 5: < 15 (kidney failure)

12. Etiology
 Most common causes of CKD are diabetes
and high blood pressure
 Other causes:
 Autoimmune diseases
 Infection-related diseases
 Sclerotic diseases
 Urinary tract infections
 Cancer

14. SIGN AND SYMPTOMS:

15. LABORATORY FINDING:

16. IMAGING:
 The finding of small, echogenic kidneys
bilaterally (less than 9–10 cm) by
ultrasonography suggests the chronic
parenchymal scarring of advanced CKD.
 Large kidneys can be seen with adult
polycystic kidney disease, diabetic
nephropathy, HIV- associated nephropathy,
plasma cell myeloma, amyloidosis, and
obstructive uropathy.

17. COMPLICATION:
 CARDIOVASCULAR COMPLICATION:
 HYPERTENSION:
Hypertension is the most common
complication of
CKD;it tends to be progressive and salt-
sensitive.
• Exogenous erythropoietin administration can
also exacerbate hypertension.
• A low salt diet (2 g/day) is often essential to
control blood pressure and help avoid overt
volume overload. Diuretics are nearly always
needed to help control hypertension.

18.  Thiazides work well in early CKD, but in
those with a GFR less than 30 mL/min/1.73
m2, loop diuretics are more effective.
 Current guidelines differ with respect to blood
pressure goals in CKD; those from the Joint
National Commission suggest a blood
pressure goal of less than 140/90 mm Hg,
while the American Heart Association
advocates for less than 130/80 mm Hg.

19.  CORONARY ARTERY DISEASE:
Patients with CKD are at higher risk for
death from CVD than the general population.
Traditional modifiable risk factors for CVD, such
as hypertension, tobacco use, and
hyperlipidemia, should be aggressively treated in
patients with CKD.

20.  HEART FAILURE:
Patients with CKD may also have accelerated
rates of atherosclerosis and vascular calcification
resulting in vessel stiffness.
• All of these factors contribute to left ventricular
hypertrophy and heart failure with preserved
ejection fraction, which is common in CKD.
• Diuretic therapy, in addition to prudent fluid and salt
restriction, is usually necessary.
• ACE inhibitors and ARBs can be used for patients
with advanced CKD with close monitoring of blood
pressure as well as for hyperkalemia and worsening
kidney function.

21.  DISORDERS OF
MINERAL
METABOLISM:
A typical pattern
seen as early as CKD
stage 3 is
hyperphosphatemia,
hypocalcemia, and
hypovitaminosis D,
resulting in secondary
hyperparathyroidism.

23. BONE CHANGES IN CKD:
 Renal osteodystrophy - common in
advanced CKD
 osteitis fibrosa cystica - Most common, is a
result of secondary hyperparathyroidism and
the osteoclast-stimulating effects of PTH
 Adynamic bone disease - it may result
iatrogenically from suppression of PTH or via
spontaneously low PTH production.
 Osteomalacia-lack of bone mineralization.

24. TREATMENT OF METABOLIC
BONE DISEASE:
 The first step in treatment of metabolic bone disease
is control of hyperphosphatemia.
 This involves dietary phosphorus restriction initially
(see section on dietary management), followed by the
administration of oral phosphorus binders if targets
are not achieved.
 Oral phosphorus binders block absorption of dietary
phosphorus in the gut and are given thrice daily with
meals.
 Once serum phosphorus levels are controlled, active
vitamin D (1,25[OH] vitamin D, or calcitriol) or
active vitamin D analogs are recommended to treat
secondary hyperparathyroidism in advanced CKD and

25. HEMATOLOGICAL
COMPLICATION:
 ANEMIA: Chronic blood loss, hemolysis, marrow
suppression by uremic factors, and reduced renal
production of EPO
 Normocytic, normochromic
 COAGULOPATHY:oagulopathy:
Clinical bleeding in uremia is typically cutaneous, including
easy bruising and mucosal bleeding, or may occur in
response to injury or invasive procedures.
Less frequent is epistaxis, gingival bleeding, or hematuria.
 Mainly platelet dysfunction – decreased activity of platelet
factor III, abnormal platelet aggregation and adhesiveness
and impaired thrombin consumption
 Increased propensity to bleed – post surgical, GI Tract,
pericardial sac, intracranial

26. TREATMENT OF ANEMIA:
 Erythropoiesis-stimulating agents (ESAs, eg,
recombinant erythropoietin [epoetin alfa or beta] and
darbepoetin) are used to treat the anemia of CKD if
other treatable causes are excluded.
 There is likely no benefit of starting an ESA before
hemoglobin (Hgb) values are less than 9 g/dL
 Raising the Hgb to 9– 10 g/dLin anemic patients can
reduce risk of bleeding via improved clot formation.
Desmopressin (25 mcg intravenously every 8–12
hours for two doses) is a short-lived but effective
treatment for platelet dysfunction and it is often used
in preparation for surgery or kidney biopsy.
 Dialysis improves the bleeding time.

27. HYPERKALEMIA:
 Cardiac monitoring is indicated for any ECG
changes seen with hyperkalemia or a serum
potassium level greater than 6.0–6.5 mEq/Lor
mmol/L.
 Chronic hyperkalemia is best treated with
dietary potassium restriction (2 g/day) and
minimization or elimination of any medications
that may impair renal potassium excretion.

29. ACID BASE DISORDERS:
 Damaged kidneys are unable to excrete the 1
mEq/kg/day of acid generated by metabolism
of dietary animal proteins in the typical
Western diet.
 The resultant metabolic acidosis is primarily
due to decreased GFR; proximal or distal
tubular defects may contribute to or worsen
the acidosis.
 Reduction in the intake of dietary animal
protein and the administration of oral
sodium bicarbonate (in doses of 0.5–1.0
mEq/kg/day divided twice daily and titrated as
needed) may achieve this goal

30. NEUROLOGICAL
COMPLICATION:
 Uremic encephalopathy, resulting from the
aggregation of uremic toxins, does not occur
until GFR falls below 5–10 mL/min/1.73 m2.
 Other neurologic complications that can
manifest with advanced CKD include
peripheral neuropathies (stocking-glove or
isolated mononeuropathies), erectile
dysfunction, autonomic dysfunction, and
restless leg syndrome. These may not
improve with dialysis therapy.

31. ENDOCRINE DISORDERS:
 There is risk of hypoglycemia in treated
diabetic patients with advanced CKD due to
decreased renal elimination of insulin.
 Doses of oral hypoglycemics and insulin may
need reduction.
 The risk of lactic acidosis with metformin is
due to both dose and eGFR; it should be
discontinued when eGFR is less than 30
mL/min/1.73 m2.
 Decreased libido and erectile dysfunction are
common in advanced CKD. Men have
decreased testosterone levels; women are
often anovulatory

32. Medical Treatment:
 Goal: to treat underlying pathophysiology to
delay progression of disease
 Control of BSR
 Control of hypertension.
 weight reduction
Several small studies suggest a possible benefit of
oral bicarbonate therapy in slowing CKD
progression when acidemia is present; treating
hyperuricemia, if present, may also retard
progression and lower blood pressure.

33. DIETARY MANAGEMENT:
 Protein restriction:
Reduced intake of animal protein to 0.6-
0.8 g/kg/day may retard CKD progression and is
likely not harmful in the otherwise well-nourished
patient
it is not advisable in those with cachexia or low
serum albumin in the absence of the nephrotic
syndrome

34.  Salt and water restriction:
A goal of 2 g/day of sodium is reasonable
for most patients. Daily fluid restriction to 2 Lmay
be needed if volume overload is present.
 Potassium restriction:
Restriction is needed once the GFR has
fallen below 10–20 mL/min/1.73 m2, or earlier if
the patient is hyperkalemic.
Limit their intake to less than 50–60 mEq/day (2
g/day).

35.  Phosphorus restriction:
Dietary phosphate restriction to 800–
1000 mg/day is the first step.
• Processed foods and cola beverages are often
preserved with highly bioavailable phosphorus
and should be avoided.
• Foods rich in phosphorus such as eggs, dairy
products, nuts, beans, and meat may also
need to be limited, although care must be
taken to avoid protein malnutrition

36.  Medication Management:
Many drugs are excreted by the kidney; dosages
should be adjusted for GFR.
• Insulin doses may need to be decreased as noted
above.
• Magnesium-containing medications, such as
laxatives or antacids, and phosphorus-containing
medicines, (eg, cathartics) should be avoided.
• Active morphine metabolites can accumulate in
advanced CKD; this problem is not encountered with
other opioid agents.
• Drugs with potential nephrotoxicity (NSAIDs,
intravenous contrast) should be avoided.

37. When GFR declines to 5–10 mL/min/1.73 m2,
renal replacement therapy (hemodialysis,
peritoneal dialysis, or kidney transplantation) is
required to sustain life.
 Dialysis:
Treatment at a hemodialysis center occurs three
times a week.
Sessions last 3–5 hours depending on patient
size and type of dialysis access. Home
hemodialysis is often performed more frequently
(3–6 days per week for shorter sessions) and
requires a trained helper.

38. PERITONEAL DIALYSIS:
peritoneal cavity is used and a dialysate in introduced
through a peritoneal catheter
 Can be performed in any clean, well-lit location
 Offers more freedom and flexibility for patient
 The most common complication of peritoneal
dialysis is peritonitis
 Staphylococcus aureus is the most common infecting
organism, but streptococci and gram-negative species
may also be causative.
 Empiric intraperitoneal administration of either
vancomycin or a first-generation cephalosporin
(cefazolin) plus a third-generation cephalosporin
(ceftazidime) should be instituted

39. Kidney Transplant
 Matches must be immunologically compatible
 After transplant patients put on
immunosuppressives
 Corticosteroids
 Cyclosporine
 Tacrolimus
 Mycophenolate mofetil
 Sirolimus

40.  Very elderly persons may die soon after
dialysis initiation; those who do not may
nonetheless rapidly lose functional status in
the first year of treatment.
 Diuretics, volume restriction, and opioids, may
help decrease the symptoms of volume
overload.
 Treatment of hyperklemia is life saving

41. Prognosis
 Overall 5-year survival is currently estimated at
40%. Patients undergoing dialysis have an average
life-expectancy of 3–5 years, but survival for as long
as 25 years may be achieved depending on
comorbidities.
 Untreated, it usually worsens to end-stage renal
disease
 Lifelong treatment may control the symptoms of
CKD