Laboratory Reference Ranges in Healthy Adults

Electrolytes

 Ammonia: 15-50 µmol/L

 Ceruloplasmin: 15-60 mg/dL
 Chloride: 95-105 mmol/L
 Copper: 70-150 µg/dL
 Creatinine: 0.8-1.3 mg/dL
 Blood urea nitrogen: 8-21 mg/dL
 Ferritin: 12-300 ng/mL (men), 12-150 ng/mL (women)
 Glucose: 65-110 mg/dL
 Inorganic phosphorous: 1-1.5 mmol/L
 Ionized calcium: 1.03-1.23 mmol/L
 Magnesium: 1.5-2 mEq/L
 Phosphate: 0.8-1.5 mmol/L
 Potassium: 3.5-5 mmol/L
 Pyruvate: 300-900 µg/dL
 Sodium: 135-145 mmol/L
 Total calcium: 2-2.6 mmol/L (8.5-10.2 mg/dL)
 Total iron-binding capacity: 45-85 µmol/L
 Total serum iron: 65-180 µg/dL (men), 30-170 µg/dL (women)
 Transferrin: 200-350 mg/dL
 Urea: 1.2-3 mmol/L
 Uric acid: 0.18-0.48 mmol/L
 Zinc: 70-100 µmol/L

Hematology

 Hemoglobin: 13-17 g/dL (men), 12-15 g/dL (women)

 Hematocrit 40%-52% (men), 36%-47%
 Glycosylated hemoglobin 4%-6%
 Mean corpuscular volume (MCV): 80-100 fL
 Red blood cell distribution width (RDW): 11.5%-14.5%
 Mean corpuscular hemoglobin (MCH): 0.4-0.5 fmol/cell
 Mean corpuscular hemoglobin concentration (MCHC): 30-35 g/dL
 Reticulocytes 0.5%-1.5%
 White blood cells (WBC) 4-10 x 10^9/L
 Neutrophils: 55-70%
 Bands: < 1 x 10^9/L
 Lymphocytes: 20–40%
 Monocytes: 2–8%
 Eosinophils: 1-4%
 Platelets: 150-400 x 10^9/L
 Prothrombin time: 11-14 sec
 International normalized ratio (INR): 0.9-1.2
 Activated partial thromboplastin time (aPTT): 20-40 sec
  Fibrinogen: 1.8-4 g/L

Lipids

 Triglycerides: 50-150 mg/dL

 Total cholesterol: 3-5.5 mmol/L
 High-density lipoprotein (HDL): 40-80 mg/dL
 Low-density lipoprotein (LDL): 85-125 mg/dL

Acid base

 pH: 7.35-7.45
 Base excess: (-3)-(+3)
 H+: 36-44 nmol/L
 Partial pressure of oxygen (pO2): 75-100 mm Hg
 Oxygen saturation: 96%-100%
 Partial pressure of carbon dioxide (pCO2): 35-45 mm Hg
 Bicarbonate (HCO3): 18-22 mmol/L

Gastrointestinal function

 Albumin: 35-50 g/L

 Alkaline phosphatase: 50-100 U/L
 Alanine aminotransferase (ALT): 5-30 U/L
 Amylase: 30-125 U/L
 Aspartate aminotransferase (AST): 5-30 U/L
 Direct bilirubin: 0-6 µmol/L
 Gamma glutamyl transferase: 6-50 U/L
 Lipase: 10-150 U/L
 Total bilirubin: 2-20 µmol/L
 Total protein: 60-80 g/L

Cardiac enzymes

 Creatine kinase: 25-200 U/L

 Creatine kinase MB (CKMB): 0-4 ng/mL
 Troponin: 0-0.4 ng/mL

Vitamins

 Folate (serum) : 7-36 nmol/L

 Vitamin A: 30-65 µg/dL
 Vitamin B12: 130-700 ng/L
 Vitamin C: 0.4-1.5 mg/dL
 Vitamin D: 5-75 ng/mL

Tumor markers
  Alpha fetoprotein: 0-44 ng/mL
 Beta human chorionic gonadotropin (HCG): < 5 IU/I
 CA19.9: < 40 U/mL
 Carcinoembryonic antigen (CEA): < 4 ug/L
 Prostatic acid phosphatase (PAP): 0-3 U/dL
 Prostate-specific antigen (PSA): < 4 ug/L

Miscellaneous

 Alpha 1-antitrypsin: 20-50 µmol/L

 Angiotensin-converting enzyme: 23-57 U/L
 C-reactive protein: < 5 mg/L
 D-dimer: < 500 ng/mL
 Erythrocyte sedimentation rate (ESR): Less than age/2 mm/hour
 Lactate dehydrogenase (LDH): 50-150 U/L
 Lead: < 40 µg/dL
 Rheumatoid factor: < 25 IU/ml

Colic is a form of pain that starts and stops abruptly. It occurs due to muscular contractions of a
hollow tube (colon, gall bladder, ureter, etc.) in an attempt to relieve an obstruction by forcing
content out. It may be accompanied by sweating and vomiting.

Types of colic in adults

There are three types of colic seen in adults.

1. Biliary colic

Biliary colic is often caused by gallstones. Gallstones are pieces of hardened digestive fluid,
called bile. This hardened fluid can form a stone-like substance and block ducts that flow
from your gallbladder to your pancreas or liver.

These blockages can cause inflammation and tenderness and lead to problems with digestion.

Symptoms include an abrupt pain that’s located either in your right side under the breastbone
or more toward the center of your abdomen. The pain intensifies over time but generally
doesn’t last for more than a few hours.

2. Renal colic

About 10 percent of the population develops renal colic at some point in their lives. This
sudden, sometimes intense pain is often associated with kidney or urinary stones.

The pain tends to be focused on the side of the body where the stones are located, and it
comes in waves. Besides pain, which can vary based on the size of the stone, other symptoms
of a urinary blockage include:

 painful urination
  bloody or foul-smelling urine
 nausea
 vomiting

3. Intestinal colic

Intestinal colic is a cramp-like pain that originates in the small or large intestine. It’s caused
by a blockage that keeps food and liquid from passing through the body. Blockages can occur
because of:

 the formation of scar tissue from previous abdominal or pelvic surgery

 inflammatory intestinal disorders like Crohn’s disease
 impacted feces
 inflamed or infected diverticula, which are the pouches that form on the wall of the
colon
 cancerous tumors

In addition to abdominal pain, symptoms include:

 the inability to have a bowel movement or pass gas

 vomiting
 loss of appetite
 abdominal distension

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Renal circulatory insuffi ciency caused by altered intra- renal hemodynamics.

a. Afferent arteriolar vasoconstriction (NSAIDs, cal- cineurin inhibitors).
 b. Efferent arteriolar vasodilation (angiotensin- converting enzyme [ACE] inhibitors,
angiotensin receptor blockers [ARBs]).

It is important to elicit a history of any of the following etiologic factors:

 Volume restriction (eg, low fluid intake, gastroenteritis)

 Nephrotoxic drug ingestion (eg, nonsteroidal anti-inflammatory drugs [NSAIDs],

aminoglycosides) [32]

 Exposure to iodinated contrast agents within the past week [32]

 Trauma or unaccustomed exertion

 Blood loss or transfusions

 Exposure to toxic substances, such as ethyl alcohol or ethylene glycol

 Exposure to mercury vapors, lead, cadmium, or other heavy metals, which can be
encountered in welders and miners

People with the following comorbid conditions are at a higher risk for developing AKI:

 Hypertension

 Chronic heart failure

 Diabetes

 Liver disease
  Obesity [33, 34, 35]

 Multiple myeloma

 Chronic infection

 Myeloproliferative disorder

 Connective tissue disorders

 Autoimmune diseases

Prerenal failure

Patients commonly present with symptoms related to hypovolemia, including thirst,

decreased urine output, dizziness, and orthostatic hypotension. Ask about volume loss from
vomiting, diarrhea, sweating, polyuria, or hemorrhage. Patients with advanced cardiac failure
leading to depressed renal perfusion may present with orthopnea and paroxysmal nocturnal
dyspnea.

Intrinsic renal failure

Patients can be divided into those with glomerular etiologies and those with tubular etiologies
of AKI. Nephritic syndrome of hematuria, edema, and hypertension indicates a glomerular
etiology for AKI. Query about prior throat or skin infections. Acute tubular necrosis (ATN)
should be suspected in any patient presenting after a period of hypotension secondary to
cardiac arrest, hemorrhage, sepsis, drug overdose, or surgery.

A careful search for exposure to nephrotoxins should include a detailed list of all current
medications and any recent radiologic examinations (ie, exposure to radiologic contrast
agents). Pigment-induced AKI should be suspected in patients with possible rhabdomyolysis
(muscular pain, recent coma, seizure, intoxication, excessive exercise, limb ischemia) or
hemolysis (recent blood transfusion). Allergic interstitial nephritis should be suspected with
fevers, rash, arthralgias, and exposure to certain medications, including NSAIDs and
antibiotics.

Postrenal failure

Postrenal failure usually occurs in older men with prostatic obstruction and symptoms of
urgency, frequency, and hesitancy. Patients may present with asymptomatic, high-grade
urinary obstruction because of the chronicity of their symptoms. A history of prior
gynecologic surgery or abdominopelvic malignancy often can be helpful in providing clues to
the level of obstruction.

Flank pain and hematuria should raise a concern about renal calculi or papillary necrosis as
the source of urinary obstruction. Use of acyclovir, methotrexate, triamterene, indinavir, or
sulfonamides implies the possibility that crystals of these medications have caused tubular
obstruction.

Initiation phase

Ischemic ATN is often described as a continuum of prerenal azotemia. Indeed, the causes of
the two conditions are the same. Ischemic ATN results when hypoperfusion overwhelms the
kidney’s autoregulatory defenses. hypoperfusion initiates cell injury

 Injury of tubular cells is most prominent in the straight portion of the proximal tubules
and in the thick ascending limb of the loop of Henle, especially as it dips into the
relatively hypoxic medulla.

 The reduction in the glomerular filtration rate (GFR) that occurs from ischemic injury
is a result not only of reduced filtration due to hypoperfusion but also of casts and
debris obstructing the tubule lumen, causing back-leak of filtrate through the damaged
epithelium (ie, ineffective filtration).

The earliest changes in the proximal tubular cells are apical blebs and loss of the brush border
membrane followed by a loss of polarity and integrity of the tight junctions. This loss of
epithelial cell barrier can result in the above-mentioned back-leak of filtrate.

Another change is relocation of Na+/K+-ATPase pumps and integrins to the apical membrane.
Cell death occurs by both necrosis and apoptosis. Sloughing of live and dead cells occurs,
leading to cast formation and obstruction of the tubular lumen (see the image below).
Activation of the renal immune system—with damage to tubular cells stimulating local
secretion of proinflammatory cytokines—in turn induces further necrosis. [3]

In addition, ischemia  decreased production of vasodilators (ie, nitric oxide, prostacyclin

[prostaglandin I2, or PGI2]) by the tubular epithelial cells  vasoconstriction and
hypoperfusion. 

On a cellular level, ischemia causes

 depletion of adenosine triphosphate (ATP), The decrease or depletion of ATP leads to

many problems with cellular function, not the least of which is active membrane
transport.

 an increase in cytosolic calcium,

 free radical formation,

 metabolism of membrane phospholipids

 abnormalities in cell volume regulation.

With ineffective membrane transport, cell volume and electrolyte regulation are disrupted 
cell swelling and intracellular accumulation of sodium and calcium. Typically, phospholipid
metabolism is altered, and membrane lipids undergo peroxidation. In addition, free radical
formation is increased, producing toxic effects. Damage inflicted by free radicals apparently
is most severe during reperfusion.

Maintenance phase

The maintenance phase of ATN is characterized by a stabilization of GFR at a very low level,
and it typically lasts 1-2 weeks. Complications (eg, uremic and others; see Complications)
typically develop during this phase.

The mechanisms of injury described above may contribute to continued nephron dysfunction,
but tubuloglomerular feedback also plays a role. Tubuloglomerular feedback in this setting
leads to constriction of afferent arterioles by the macula densa cells, which detect an
increased salt load in the distal tubules.

Recovery phase

The recovery phase of ATN is characterized by regeneration of tubular epithelial cells. [4]
During recovery, an abnormal diuresis sometimes occurs, causing salt and water loss and
volume depletion. The mechanism of the diuresis is not completely understood, but it may in
part be due to the delayed recovery of tubular cell function in the setting of increased
glomerular filtration. In addition, continued use of diuretics (often administered during
initiation and maintenance phases) may also add to the problem.

Causes of ischemic acute tubular necrosis

 Hypovolemic states: Hemorrhage, volume depletion from gastrointestinal (GI) or

renal losses, burns, fluid sequestration

 Low cardiac output states: Heart failure and other diseases of myocardium,
valvulopathy, arrhythmia, pericardial diseases, tamponade

 Systemic vasodilation: Sepsis, anaphylaxis

 Disseminated intravascular coagulation

the incidence of AKI was 577 per 100,000 population

Hyperkalemia
 Hyperkalemia is most commonly seen in patients with end-stage renal disease.
TABLE. Common Causes of Hyperkalemia
Endogenous Causes
    • Chronic renal failure
    • Metabolic acidosis (eg, diabetic ketoacidosis)
    • Pseudohypoaldosteronism type II (also known as Gordon’s syndrome; familial
hyperkalemia and hypertension)
    • Chemotherapy causing tumor lysis
    • Muscle breakdown (rhabdomyolysis)
    • Renal tubular acidosis
    • Hemolysis
    • Hypoaldosteronism (Addison’s disease, hyporeninemia)
    • Hyperkalemic periodic paralysis
Exogenous Causes
    • Medications: K+-sparing diuretics, ACE inhibitors, nonsteroidal anti-
inflammatory drugs, potassium supplements, penicillin derivatives, succinylcholine, heparin
therapy (especially in patients with other risk factors), β-blockers
    • Blood administration (particularly with large transfusions of older “bank” blood)
    • Diet (rarely the sole cause), salt substitutes
    • Pseudohyperkalemia (due to blood sampling or hemolysis, high white blood cell
count, high platelets, tumor lysis syndrome)

Signs and symptoms of hyperkalemia include weakness, ascending paralysis, and respiratory
failure. A variety of electrocardiographic (ECG) changes suggest hyperkalemia. Early
findings include peaked T waves (tenting). As the serum potassium rises further, flattened P
waves, prolonged PR interval (first-degree heart block), widened QRS complex, deepened S
waves, and merging of S and T waves can be seen. If hyperkalemia is left untreated, a sine-
wave pattern, idioventricular rhythms, and asystolic cardiac arrest may develop.

Hypokalemia
The most common causes of low serum potassium are gastrointestinal loss (diarrhea,
laxatives), renal loss (hyperaldosteronism, severe hyperglycemia, potassium-depleting
diuretics, carbenicillin, sodium penicillin, amphotericin B), intracellular shift (alkalosis or a
rise in pH), and malnutrition.
The major consequences of severe hypokalemia result from its effects on nerves and muscles
(including the heart). The myocardium is extremely sensitive to the effects of hypokalemia,
particularly if the patient has coronary artery disease or is taking a digitalis derivative.
Symptoms of mild hypokalemia are weakness, fatigue, paralysis, respiratory difficulty,
constipation, paralytic ileus, and leg cramps; more severe hypokalemia will alter cardiac
tissue excitability and conduction. Hypokalemia can produce ECG changes such as U waves,
T-wave flattening, and arrhythmias (especially if the patient is taking digoxin), particularly
ventricular arrhythmias. Pulseless electrical activity or asystole may develop.

Hypernatremia
It may be caused by a primary gain in Na+ or excess loss of water. Gains in sodium can
result from hyperaldosteronism (excess mineralocorticoid), Cushing’s syndrome (excess
glucocorticoid), or excessive hypertonic saline or sodium bicarbonate administration. Loss of
free water can result from gastrointestinal losses or renal excretion (eg, osmotic diuresis or
diabetes insipidus).
Hypernatremia may cause neurologic symptoms such as altered mental status, weakness,
irritability, focal neurologic deficits, and even coma or seizures. The severity of symptoms is
determined by the speed and magnitude of the change in serum sodium concentration.

Hyponatremia
It is caused by an excess of water relative to sodium. Most cases of hyponatremia are caused
by reduced renal excretion of water with continued water intake or by loss of sodium in the
urine. Impairment of renal water excretion may be caused by
• Use of thiazide diuretics
• Renal failure
• ECF depletion (eg, vomiting with continued water intake)
• Syndrome of inappropriate antidiuretic hormone (SIADH) secretion
• Edematous states (eg, congestive heart failure, cirrhosis with ascites)
• Hypothyroidism
• Adrenal insufficiency
Most cases of hyponatremia are associated with low serum osmolality (so-called hypo-
osmolar hyponatremia). Hyponatremia is usually asymptomatic unless it is acute or severe
(<120 mEq/L). An abrupt fall in serum sodium produces a free water shift from the vascular
to the interstitial space that can cause cerebral edema. In this case the patient may present
with nausea, vomiting, headache, irritability, lethargy, seizures, coma, or even death.

Hypermagnesemia
The most common cause of hypermagnesemia is renal failure.
Neurologic symptoms of hypermagnesemia are muscular weakness, paralysis, ataxia,
drowsiness, and confusion. Moderate hypermagnesemia can produce vasodilation; severe
hypermagnesemia can produce hypotension. Extremely high serum magnesium levels may
produce a depressed level of consciousness, bradycardia, cardiac arrhythmias,
hypoventilation, and cardiorespiratory arrest.15

Hypomagnesemia
Hypomagnesemia usually results from decreased absorption or increased loss of magnesium
from either the kidneys or intestines (diarrhea). Alterations in thyroid hormone function and
certain medications (eg, pentamidine, diuretics, alcohol) can also induce hypomagnesemia.
Hypomagnesemia interferes with the effects of parathyroid hormone, resulting in
hypocalcemia. It may also cause hypokalemia.
Symptoms of low serum magnesium are muscular tremors and fasciculations, ocular
nystagmus, tetany, altered mental state, and cardiac arrhythmias such as torsades de pointes
(multifocal ventricular tachycardia). Other possible symptoms are ataxia, vertigo, seizures,
and dysphagia.

Hypercalcemia
Hypercalcemia is defined as a total serum calcium concentration >10.5 mEq/L (or an
elevation in ionized calcium >4.8 mg/dL). Primary hyperparathyroidism and malignancy
account for >90% of reported cases.17 In these and most forms of hypercalcemia, release of
calcium from the bones and intestines is increased, and renal clearance may be compromised.
Symptoms of hypercalcemia usually develop when the total serum calcium concentration is
≥12 to 15 mg/dL. Neurologic symptoms are depression, weakness, fatigue, and confusion at
lower levels. At higher levels patients may experience hallucinations, disorientation,
hypotonicity, seizures, and coma. Hypercalcemia interferes with renal concentration of urine;
the diuresis can cause dehydration.
Cardiovascular symptoms of hypercalcemia are variable. Myocardial contractility may
initially increase. Automaticity is decreased and ventricular systole is shortened. Arrhythmias
occur. Hypercalcemia can worsen digitalis toxicity and may cause hypertension. In addition,
many patients with hypercalcemia develop hypokalemia.
Gastrointestinal symptoms of hypercalcemia include dysphagia, constipation, peptic ulcers,
and pancreatitis. Effects on the kidney include diminished ability to concentrate urine;
diuresis, leading to loss of sodium, potassium, magnesium, and phosphate; and a vicious
cycle of calcium absorption in the intestines and calcium release from the bones that worsens
hypercalcemia.

Hypocalcemia
Hypocalcemia is defined as a serum calcium concentration <8.5 mg/dL (or ionized calcium
<4.2 mg/dL). Hypocalcemia may develop with toxic shock syndrome, with abnormalities in
serum magnesium, after thyroid surgery, with fluoride poisoning, and with tumor lysis
syndrome (rapid cell turnover with resultant hyperkalemia, hyperphosphatemia, and
hypocalcemia).
Symptoms of hypocalcemia usually occur when ionized levels fall to <2.5 mg/dL. Symptoms
include paresthesias of the extremities and face, followed by muscle cramps, carpopedal
spasm, stridor, tetany, and seizures. Hypocalcemic patients show hyperreflexia and positive
Chvostek and Trousseau signs. Cardiac effects include decreased myocardial contractility and
heart failure. Hypocalcemia can exacerbate digitalis toxicity.