2. LSM, 61/F
Married
Metro Manila
Admitted: 7/17/19
General
Data
Chief
Complain
t
Past
Medical
History
Family
Medical
History
Personal
& Social
History
Review of
Systems
4. 2 Years PTA
2 Months PTA
1 Month PTA
Few Hours PTA
● Known case of Type II Diabetes Mellitus 35 years prior to admission
○ Maintained on Insulin glargine
■ Poor compliance
○ Glimepiride was subsequently added after 5 years
■ Good compliance
● No known signs and symptoms until
5. 2 Years PTA
2 Months PTA
1 Month PTA
Few Hours PTA
● (+) Numbness of lower extremities
● (+) Bipedal edema resolved when lying down
● (+) 2-pillow Orthopnea
● (+) Occasional dyspnea
● Sought consult at St. Victoria’s Hospital and was noted to have elevated serum
creatinine level
○ Glimepiride removed for her medications
○ Linagliptin (Tradjenta) 5mg OD added
○ Losartan 50 mg OD
■ Diagnosed with Hypertension Stage 1
○ Allegedly had good compliance
6. 2 Years PTA
2 Months PTA
1 Month PTA
Few Hours PTA
● (+) Non-healing wound on right foot
● (+) Edema
● (+) Parasthesias of bilateral hands
● No consult done, no additional meds taken
7. 2 Years PTA
2 Months PTA
1 Month PTA
Few Hours PTA
● Right foot wound was noted to be foul-smelling
○ (+) Swelling
○ (+) wound increased in size
● Sought consult at St. Anthony Medical Center
○ Managed as a case of DM foot
○ S/P amputation of left foot (6/26/2019)
○ On admission, creatinine level was at 148 ug/dL
○ Day 5 of admission, creatinine level was at 462 ug/dL
■ Advised for hemodialysis
● DAMA
8. 2 Years PTA
2 Months PTA
1 Month PTA
Few Hours PTA
● Sought second opinion to Dr. Manlutac at OPD
● On her way to the clinic, patient suddenly experienced difficulty of
breathing hence consult at the ER and subsequent admission
17. Differential Diagnoses
MORE LIKELY LESS LIKELY
Known case of Hypertension Stage I with previous history of
poor compliance to med
Difficulty of Breathing
2-pillow orthopnea
Strong family history of hypertension (father)
BP 150/90
Grade 1 bilateral upper extremity edema
Globular abdomen
Bibasal crackles
Oliguric
(-) Neck vein distention
(-) Extra heart sounds
(-) Hepatomegaly
CONGESTIVE HEART FAILURE SECONDARY TO HYPERTENSIVE ARTERIOSCLEROTIC
CARDIOVASCULAR DISEASE
18. Differential Diagnoses
MORE LIKELY LESS LIKELY
Known case of Hypertension Stage I with previous history of
poor compliance to med
Sudden onset difficulty of breathing
Strong family history of hypertension (father)
BP 150/90
(-) Chest pain
(-) Diaphoresis
(-) Anxiety, restlessness
(-) Pale cool skin
(-) Sinus tachycardia
(-) Extra heart sounds
ACUTE CORONARY SYNDROME
19. Differential Diagnoses
MORE LIKELY LESS LIKELY
s/p Amputation
Sudden onset of difficulty of breathing
Occassional dry cough
(-) Tachypnea
CARDIOPULMONARY EMBOLISM
20. Day 1
S O A P
(+) Dyspnea
(-) Chest pain
Awake, weak-looking, in
wheelchair, not in
cardiorespiratory
distress
BP 150/80, HR 79, RR
20, Temp 37 C
Anicteric sclerae, pink
palpebral conjunctiva,
(+) Bibasal crackles,
Adynamic precordium, (-
) murmurs
(+) Globular abdomen
(+) Grade 2 upper
extremities edema
Acute Kidney Injury on
top of chronic kidney
disease sec to diabetic
kidney disease; Hospital
acquired pneumonia
Admitted
Diagnostics: CBC, BUN,
Crea, Na, K, Cl, Alb,
Phos, Aptt, HbsAg, Anti-
HCv, Anti Hbs, CXR,ECG,
Sputum GS
Therapeutics:
Ceftazidine 2g,
Amlodipine 10 mg/tab ,
Cimetidine 150
mcg/tab, Pregabalin
75mg/tab, Linagliptin
5mg/tab,
21. S O A P
Decrease in dyspnea
(-) Chest pain
BP 160/80, HR 92, RR
20, Temp 36.7
Rales right base, left
mid, Adynamic
precordium, (-) Murmur
(+) Grade 1 upper
extremities edema
Alb 2.8, BUN 58, Crea
1.8(Egfr: 29) Ca 8, Phos
5.4, K 6.2, HC03 29.7,
Na 120
UO: 47 CC/hr
CXR: cardiomegaly, with
congestion
CHF
Hyperkalemia
Hyponatremia
Repeat Na, K
For 2D echo
Furosemide 20mg/iv,
calcium gluconate,
kalimate sachet,
metoclopramide,
paracetamol 500mg/tab
Start PNSS
Day 2
22. S O A P
(+) Orthopnea
(+) Chest heaviness
relieved after placing on
high backrest
BP 130/80, HR 87, RR
19, Temp 37
Conscious, cooperative
Pink PC, AS, Bilateral
crackles
Grade 2 edema
2d Echo: EF 62%
CHF sec to HSCVD
CKD
ISDN 5mg SL
Repeat Na, K, Cl
Day 3
23. S O A P
Decrease dyspnea &
orthopnea
Awake, cooperative,
comfortable
BP 140/80, PR 80, RR
20, Temp 36.5
Anicteric sclerae, Pink
PC, Decreased bibasal
crackles, Gr. 1 edema
K 5.2, Na127, Crea 1.8
CHF sec to HSCVD
CKD
Start D50/50
Day 4
25. • Sudden impairment of kidney function resulting in the retention of
nitrogenous and other waste products normally cleared by the kidneys
• Designation for a heterogeneous group of conditions that share common
diagnostic features:
- Increase in the blood urea nitrogen (BUN) concentration
- Increase in the plasma or serum creatinine
- Reduction in urine volume
• Classified based on severity—stages 1 through 3—and location of injury:
prerenal, intrinsic renal, or postrenal
ACUTE KIDNEY INJURY
26. • Condition is defined by an increase in serum creatinine level or a decrease in
urine output. According to the KDIGO (Kidney Disease: Improving Global
Outcomes) international guidelines, 1 of the following must be present:
○ Increase in serum creatinine level of 0.3 mg/dL or more within 48 hours
○ Increase in serum creatinine level to 1.5 times the baseline or more
within 7 days
○ Decrease in urine output less than 0.5 mL/kg/hour for 6 hours
ACUTE KIDNEY INJURY
27. Data from Acute Kidney Injury Work Group: Kidney Disease: Improving Global Outcomes (KDIGO): clinical practice guideline for acute
kidney injury. Kidney Int. 2(Suppl 1):1-138, 2012.
ACUTE KIDNEY INJURY
28. • Classification by Cause
✔ Prerenal - Renal dysfunction without structural injury to the renal parenchyma
✔ Intrinsic - Renal dysfunction due to injury to the tubules, glomeruli, interstitium,
and intrarenal blood vessels
✔ Postrenal - Renal dysfunction due to an acute obstruction to urinary flow
ACUTE KIDNEY INJURY
29.
30. PRE- RENAL AKI
- Decreased blood flow
1. ABSOLUTE loss of fluid
- Major hemorrhage
- Vomiting
- Diarrhea
- Severe burns
2. RELATIVE loss of fluid
- Distributive shock
- Congestive Heart Failure
ACUTE KIDNEY INJURY
3. Renal artery occlusion
4. Systemic vasodilation
5. Afferent arteriolar constriction
6. Efferent arteriolar dilation
Decreased renal
filtration pressure
31. PRE- RENAL
ACUTE KIDNEY INJURY
Decreased blood flow
to the kidneys (e.g.
volume depletion,
hypotension)
Decreased renal
filtration pressure
Decreased blood
filtered
Decreased GFR
Increased BUN
Increased Creatinine
AZOTEMIA
Oliguria
Activate RAAS
32. ACUTE KIDNEY INJURY
Activate RAAS
Release of
aldosterone
Na reabsorption
Water reabsorption
More increased in
BUN = BUN:
creatinine ratio >20:1
Oliguria/edema
Urine Na <20 mEq/L
FENa <1%
Uosm > 500 mOsm/kg
Severe Pre- renal azotemia may lead to
ISCHEMIA in the tubules which can cause
ATN and may manifest as Intrinsic AKI.
33. Clinical Presentation
✔ Varies with cause and severity of renal injury, as well as associated diseases
✔ In early stages, patients are often asymptomatic
✔ In advanced stages, patients may experience any of the following:
○ Vomiting and/or diarrhea
○ Extreme thirst, muscle cramps, and other signs of dehydration
○ Edematous legs, ankles, and feet
○ Flank or abdominal pain, indicative of an obstruction or occlusion
○ Decreased frequency of urination or force of urine flow
ACUTE KIDNEY INJURY
34. Physical Examination
✔ Signs of hypovolemia or hypervolemia can occur in acute kidney injury
✔ Signs of hypovolemia include tachycardia, orthostatic and/or supine hypotension,
dry mucous membranes, decreased skin turgor, cool extremities, and sunken eyes
✔ Signs of hypervolemia include edema and weight gain
✔ Reduced urine output - anuria or oliguria in hospitalized patients, although some
patients may be nonoliguric
ACUTE KIDNEY INJURY
35. Urine Findings
✔ Complete anuria early in the course of AKI is uncommon
✔ A reduction in urine output (oliguria, defined as <400 mL/24 h) usually denotes
more severe AKI (i.e., lower GFR) than when urine output is preserved.
✔ Red or brown urine may be seen with or without gross hematuria; if the color
persists in the supernatant after centrifugation, then pigment nephropathy from
rhabdomyolysis or hemolysis should be suspected.
ACUTE KIDNEY INJURY
36. Urine Findings
✔ In the absence of preexisting proteinuria from CKD, AKI from ischemia or
nephrotoxins leads to mild proteinuria (<1 g/d).
✔ Prerenal azotemia may present with hyaline casts
✔ Postrenal AKI may also lead to an unremarkable sediment, but hematuria and
pyuria may be seen depending on the cause of obstruction.
✔ AKI from ATN has characteristic urine sediment findings: pigmented “muddy
brown” granular casts and tubular epithelial cell casts.
ACUTE KIDNEY INJURY
37. Urine Findings
✔ Glomerulonephritis may lead to dysmorphic red blood cells or red blood cell
casts.
✔ Interstitial nephritis may lead to white blood cell casts.
✔ Crystalluria may be important diagnostically. The finding of oxalate crystals in
AKI should prompt an evaluation for ethylene glycol toxicity.
✔ Abundant uric acid crystals may be seen in the tumor lysis syndrome.
ACUTE KIDNEY INJURY
38.
39. Laboratory Findings
✔ Prerenal azotemia typically leads to modest rises in SCr that return to baseline
with improvement in hemodynamic status.
✔ Contrast nephropathy leads to a rise in SCr within 24–48 h, peak within 3–5
days, and resolution within 5–7 days. In comparison
✔ Anemia is common in AKI and is usually multifactorial in origin.
✔ AKI often leads to hyperkalemia, hyperphosphatemia, and hypocalcemia.
✔ Marked hyperphosphatemia with accompanying hypocalcemia suggests
rhabdomyolysis or the tumor lysis syndrome
ACUTE KIDNEY INJURY
40. Kidney damage for ≥3 months, as defined by structural or functional abnormalities
of the kidney, with or without decreased GFR, that can lead to decreased GFR,
manifest by either:
• Pathologic abnormalities
• Markers of kidney damage, including abnormalities in the composition of blood
or urine, or abnormalities in imaging tests
• GFR <60 ml/min/1.73 m2 for ≥3 months, with or without kidney damage
CHRONIC KIDNEY DISEASE
44. Pathophysiology of CKD
The pathophysiology of CKD involves two broad sets
of mechanisms of damage:
(1) initiating mechanisms specific to the underlying etiology
(2) a set of progressive mechanisms involving hyperfiltration and
hypertrophy of the remaining viable nephrons
Maladaptive
distortion of glomerular architecture
abnormal podocyte function
disruption of the filtration barrier
sclerosis and dropout of the remaining nephrons
CHRONIC KIDNEY DISEASE
47. Risk Factors
• small for gestation birth weight
• Childhood obesity
• Hypertension
• diabetes mellitus
• Autoimmune disease
• advanced age
• African ancestry
• a family history of kidney disease,
• a previous episode of acute kidney injury
• presence of proteinuria, abnormal urinary sediment, or structural abnormalities of
the urinary tract.
CHRONIC KIDNEY DISEASE
48. Clinical Presentation
• Skin pallor, ecchymosis.
• Sleep disorder
• Hypertension.
• Edema, leg cramps, restless legs, peripheral neuropathy.
• Emotional lability, depression, decreased cognitive function.
• Clinical presentation varies with the degree of kidney disease and its underlying
etiology. Common symptoms are generalized fatigue, nausea, anorexia, pruritus,
sleep disturbances, smell and taste disturbances, hiccups, and seizures.
CHRONIC KIDNEY DISEASE
49. Uremia
• Uremia leads to disturbances in the function of virtually every organ system
• Chronic dialysis can reduce the incidence and severity of many of these
disturbances
• However, even optimal dialysis therapy is not completely effective as renal
replacement therapy, because some disturbances resulting from impaired kidney
function fail to respond to dialysis
CHRONIC KIDNEY DISEASE
50. Sodium and water homeostasis
• In most patients with stable CKD, the total-body content of sodium and water is
modestly increased
• dietary intake of sodium exceeds its urinary excretion, leading to sodium
retention and attendant extracellular fluid volume (ECFV) expansion.
• This expansion may contribute to hypertension
• The patient with ECFV expansion (peripheral edema, sometimes hypertension
poorly responsive to therapy) should be counseled regarding salt restriction.
CHRONIC KIDNEY DISEASE
51. Potassium homeostasis
• hyperkalemia may be precipitated in certain settings. These include increased
dietary potassium intake, protein catabolism, hemolysis, hemorrhage, transfusion
of stored red blood cells, and metabolic acidosis.
• Hypokalemia is not common in CKD and usually reflects markedly reduced dietary
potassium intake, especially in association with excessive diuretic therapy or
concurrent GI losses.
CHRONIC KIDNEY DISEASE
52. Metabolic Acidosis
• Metabolic acidosis is a common disturbance in advanced CKD.
• The majority of patients can still acidify the urine, but they produce less ammonia
and, therefore, cannot excrete the normal quantity of protons in combination with
this urinary buffer.
• The combination of hyperkalemia and hyperchloremic metabolic acidosis is often
present, even at earlier stages of CKD (stages 1–3)
• Alkali supplementation may attenuate the catabolic state and possibly slow CKD
progression and accordingly is recommended when the serum bicarbonate
concentration falls below 20–23 mmol/L.
CHRONIC KIDNEY DISEASE
53. Bone Manifestations
• Hyperparathyroidism stimulates bone turnover and leads to osteitis fibrosa
cystica. Bone histology shows abnormal osteoid, bone and bone marrow fibrosis,
and in advanced stages, the formation of bone cysts, sometimes with hemorrhagic
elements so that they appear brown in color
• Clinical manifestations of severe hyperparathyroidism include bone pain and
fragility, brown tumors, compression syndromes, and erythropoietin resistance in
part related to the bone marrow fibrosis.
• Low-turnover bone disease can be grouped into two categories—adynamic bone
disease and osteomalacia
CHRONIC KIDNEY DISEASE
54. Cardiovascular Manifestations
• Hypertension - may be “volume dependent” secondary to salt and water retention
or “renin dependent” due to activation of renin/angiotensin system.
• Congestive heart failure - salt and water retention, anemia, hypertension,
atherosclerosis
• Pericarditis - may be complicated by tamponade (12-55% of cases) and, later
stages, by constrictive pericarditis.
• Vascular calcification - may lead to gangrene.
• Atherosclerosis - accelerated due to high VLDL and low HDL and accounts for 50%
of deaths in uremic patients.
CHRONIC KIDNEY DISEASE
56. Other Manifestations
• Gastrointestinal system:
- Oral, esophagus - stomatitis, esophagitis
- Gastroduodenal - UGI hemorrhage
- Colon - constipation, ulceration, pseudomembranous colitis
- Miscellaneous - nausea, vomiting, singultus
• Dermatological
• - Pruritus - 86% of patients: due to xerosis, Ca X P product, PTH, uremic
polyneuropathy, number of mast cells.
- Skin pigmentation – urochromes deposited in skin, increase in melanin,
porphyria cutanea tarda, hemosiderosis.
- Purpura
CHRONIC KIDNEY DISEASE
57. Other Manifestations
• Hematological
- Anemia - decreased production of erythropoetin; decrease red cell survival,
50-70 days instead of the normal 120 days; dietary deficiency of iron, folate.
- Bleeding - qualitative platelet function defect; increased capillary
permeability; abnormal bleeding time: normal PT, PTT and platelet count.
- WBC - decreased phagocytic function; abnormal cellular immunity – Staph,
gram negative sepsis.
CHRONIC KIDNEY DISEASE
58. Other Manifestations
• Endocrine and metabolic systems
- Carbohydrate metabolism - abnormal GTT; due to decreased release of
insulin, increased sensitivity to insulin, increase glucagon release; increase half-
life of insulin insulin requirements in uremia; glycogen depletion due to
starvation, gluconeogenesis.
- Lipid metabolism - hyperlipidemia; triglycerides VLDL, HDL cholesterol.
CHRONIC KIDNEY DISEASE
59. Treatment
• Slow the progression of CKD
• Reducing the intraglomerular hypertension and proteinuria
○ ACEI/ARBs- renoprotective
• Medication dose adjustment
• Renal Replacement Therapy
○ Hemodialysis
○ Peritoneal Dialysis
○ Transplantation
CHRONIC KIDNEY DISEASE
60. Treatment
• It is generally better to initiate chronic dialysis before the patient is severely ill
from uremia. It is better to start a few weeks too early, than a few days too late.
• Indications for dialysis include:
a. Asymptomatic, but serum creatinine > 12 mg/dl; Creatinine clearance , 3-5
ml/min; Diabetic and serum creatinine > 8 mg/dl.
b. Uremic complication: pericarditis; neuropathy; encephalopathy; anorexia,
nausea, vomiting.
c. Volume retention with unresponsiveness to diuretic therapy.
d. Hyperkalemia not managed with diet.
e. Metabolic acidosis - not manageable with NaHCO3.
CHRONIC KIDNEY DISEASE
61. CHRONIC KIDNEY DISEASE
Treatment
• Kidney transplantation offers the best potential for complete rehabilitation,
because dialysis replaces only a small fraction of the kidneys’ filtration function
and none of the other renal functions, including endocrine and antiinflammatory
effects.
• Generally, kidney transplantation follows a period of dialysis treatment, although
preemptive kidney transplantation (usually from a living donor) can be carried out
if it is certain that the renal failure is irreversible.
62. ELECTROLYTE IMBALANCE
● Major electrolytes are Na, K, Ca, Mg
● Some are primarily extracellular (Na) and others primarily intracellular (K, Mg)
● Functions range from maintenance of intravascular volume, maintenance of cell
membrane and cellular functions (especially for Calcium and Magnesium, and the
interplay between NA and K), etc.
63. ELECTROLYTE IMBALANCE
SODIUM DISORDERS
● 85-90% of Na is extracellular
● Actively maintained by Na-K ATPase pump of cells, renal excretion, GI intake and losses
● Most important function: Primary determinant of serum osmolality
● Usually reflects ECF volume (with total body water)
● Issues regarding fluid volume and osmolality- responsive to ADH and aldosterone
● Normal serum sodium: 140 (135-145)
64. ELECTROLYTE IMBALANCE
HYPONATREMIA
● Serum Na < 135 mmol/liter
● Excessive intake of solute free water, poor excretion of excess water (edematous
patients), SIADH, excessive renal solute loss
● Usually reflects a hypo-osmolar state and an increased ICF volume
● Causes generalized cellular swelling
67. ELECTROLYTE IMBALANCE
POTASSIUM DISORDERS
● Majority (98%) of total body K is intracellular ~3,300 mEqs ECF K is ~65 mEqs
● Homeostatic mechanisms maintain serum K levels between 3.5-5.0 mmol/L
● Most important is the Na,K ATPase pump (found in all cells)
● Maintains the resting membrane potential difference between the ICF compartments and
the ECF for proper functioning of muscle, nerve, liver, etc.
68. ELECTROLYTE IMBALANCE
HYPERKALEMIA
● It is caused by excessive intake (iatrogenic), transcellular shift, and decrease in renal K +
excretion is the most common underlying cause
● Drugs that have an impact on the renin-angiotensin-aldosterone axis are also a major
cause of hyperkalemia.
● It causes cardiac toxicity presenting as ECG changes and later arrhythmias
69. ELECTROLYTE IMBALANCE
CLINICAL MANIFESTATIONS
● Cardiac arrhythmias associated with hyperkalemia include sinus bradycardia, sinus arrest,
slow idioventricular rhythms, ventricular tachycardia, ventricular fibrillation, and asystole.
● ECG manifestations:
○ Tall peaked T waves (5.5–6.5 m M )
○ Loss of P waves (6.5–7.5 m M )
○ Widened QRS complex (7–8 m M )
○ Sine wave pattern (8 m M)
72. 1. Optimization of systemic and renal hemodynamic through volume
resuscitation and judicious use of vasopressors.
2. Elimination of nephrotoxic agents (e.g., ACE inhibitors, ARBs, NSAIDs,
aminoglycosides) if possible.
3. Initiation of renal replacement therapy when indicated
General Issues
ACUTE KIDNEY INJURY
General Issues
73.
74.
75. Supportive Measures
✔ Volume Management: hypervolemia in oliguric or anuric AKI may be life
threatening due to acute pulmonary edema. Fluid and sodium should be
restricted, and diuretics may be used to increase the urinary flow rate.
✔ Electrolyte And Acid-Base Abnormalities: Acidosis can be treated with oral or
intravenous sodium bicarbonate, but overcorrection should be avoided because
of the possibility of metabolic alkalosis, hypocalcemia, hypokalemia, and volume
overload.
ACUTE KIDNEY INJURY
76. Supportive Measures
✔ Hyperphosphatemia is common in AKI and can usually be treated by limiting
intestinal absorption of phosphate using phosphate binders (calcium carbonate,
calcium acetate, lanthanum, sevelamer, or aluminum hydroxide)
✔ Malnutrition: protein energy wasting is common in AKI. Inadequate nutrition
may lead to starvation ketoacidosis and protein catabolism. Excessive nutrition
may increase the generation of nitrogenous waste and lead to worsening
azotemia.
ACUTE KIDNEY INJURY
77. Supportive Measures
✔ Protein intake should vary depending on the severity of AKI: 0.8–1.0 g/kg per
day in non-catabolic AKI without the need for dialysis; 1.0–1.5 g/ kg per day in
patients on dialysis
✔ Anemia: the anemia seen in AKI is usually multifactorial and is not improved by
erythropoiesis-stimulating agents
✔ Glycemic control: Tight glycemic control can reduce the incidence and severity
of AKI. Insulin therapy targeting plasma glucose 110-149 mg/dl.
ACUTE KIDNEY INJURY
79. ACUTE KIDNEY INJURY
Outcomes and Prognosis
✔ The development of AKI is associated with increased risk of in-hospital and long-
term mortality, longer length of stay, and increased costs.
✔ Prerenal azotemia, with the exception of the cardiorenal and hepatorenal
syndromes, and postrenal azotemia carry a better prognosis than most cases of
intrinsic AKI.
✔ Survivors of an episode of AKI requiring temporary dialysis are at extremely high
risk for progressive CKD, and up to 10% may develop end-stage renal disease.
