The document reviews uremia and uremic syndrome, emphasizing their clinical manifestations and underlying pathophysiology associated with chronic kidney failure (CKD) and acute kidney injury (AKI). It discusses the symptoms, risks, and complications, as well as diagnostic criteria and treatment options. Additionally, it covers the role of various disturbances in fluid, electrolytes, and metabolism that patients may experience due to these conditions.

1. 2020
DTMU
Vedica Sethi
[UREMIA AND UREMIC
SYNDROME]
The paper reviews Uremia and Uremic Syndrome with basic presentation of the given topic as well
as the detailed discussion about the symptoms and underlying pathophysiology.

2. Table of contents:
1. Abstract
2. What is Uremia and Uremic Syndrome?
(i) Etiology
(ii) Risk factors of CKD or ESRD
(iii) Patho- Physiology
(iv) What is CKD?
(v) Uremia solutes
3. Clinical abnormalities in Uremia:
(i) Fluid and electrolyte disturbances
(ii) Endocrine-metabolic disturbances
(iii) Neuromuscular disturbances
(iv) Cardiovascular and pulmonary disturbances
(v) Dermatologic disturbances
(vi) Gastrointestinal disturbances
(vii) Hematologic and immunologic disturbances
(viii) What is Residual Syndrome?
4. Diagnosis
5. Treatment
6. Conclusion
7. References

3. 1. Abstract
Uremia is a clinical manifestation of chronic kidney failure (CKD) and is defined as the elevation
of urea levels in plasma associated to fluid, electrolytes and hormonal imbalances and
metabolic abnormalities. Uremia even though arises from CKD, it can also occur with Acute
Kidney injury (AKI). The terms uremia was first coined by Piorry which translates to urine in
blood. Also, Uremia and uremic syndrome have been used interchangeably for a long time.
Comparatively, Azotemia is also uremia but the only difference is that the urea elevation in
azotemia is not high enough to have manifesting signs or symptoms. Thus, Uremia is
pathological and symptomatic manifestations of severe azotemia.
Urea itself has direct and indirect toxic effects on our body; parathyroid hormone (PTH), beta2
microglobulin, polyamines, advanced glycosylation end products, and other middle molecules,
are thought to contribute to the clinical syndrome. Patient’s symptoms range from mild bleeds
to severe congestive heart failure. If left untreated complicationsinclude seizure, coma, cardiac
arrest, and death. He most severe is cardiac arrest secondary to electrolyte abnormalities such
as hyperkalemia, metabolic acidosis, or hypocalcemia. The patients, who are diabetic, tend to
develop severe hypoglycemic reactions if the medications are not adjusted for creatinine
clearance. Renal failure and renal osteodystrophy may cause early onset osteoporosis or
formation of adynamic bone which predisposes the patient to fractures on mild trauma. Also
medications the patient was previously on can lead to unwanted side effects due to impaired
clearance e.g. Digoxin toxicity secondary to renal failure, increased sensitivity to narcotics.
Key Words: Uremia, Uremic syndrome, Chronic kidney failure, azotemia, beta 2 microglobulins,
congestive heart failure, electrolyte abnormalities, hyperkalemia, hyocalcemia, metabolic
acidosis, creatinine, osteodystrophy

4. 2. What is Uremia and Uremic Syndrome?
Amino acids and protein metabolismleads to the formation of the end product urea, which is then
excreted in the urine. Thus, uremia is defined as elevated concentrations of urea in blood that
would be normally excreted in the urine. Comparatively, Uremic syndrome is a clinical
manifestation of chronic kidney failure. Both the terms Uremia and Uremic Syndrome are
interchangeably used to define elevated plasma levels of urea in blood that is the result of renal
failure. Azotemia, is less severeformof uremia, where the blood concentration of urea is elevated,
but not elevated enough to produce symptoms. Thus, Uremia is pathological and symptomatic
manifestations of severe azotemia.
All patients with renal disease should undergo an assessment of renal function based on the
Glomerular filtration rate (GFR) and the measurement should be clinically used to identify the
degree of renal impairement to follow the course of the disease and response to therapy. An
attempt should be made to identify the diagnosis based on careful urinalysis, kidney ultrasound,
kidney biopsy (if necessary) and referral to a nephrologist. (1)
(i) Etiology-
The most common cause of ESRD in USA is Diabetes Mellitus and least common
causes are hypertension, glomerulonephritis, interstitial disease, cystitis, and
neoplasms.
Kidney disease can be caused from conditions ranging from:
 Primary Renal disorders- IgA nephropathy, focal segmental glomerulosclerosis,
membranoproliferative glomerulonephritis, polycystic kidney disease
 Systemic disorders- Diabetes mellitus, lupus, multiple myeloma, amyloidosis,
Goodpasture disease, Thrombotic thrombocytopenic purpura, or hemolytic
uremic syndrome.
(ii) Risk factors to CKD or ESRD are-
 Hypertension
 Diabetes Melitus
 Auto-immune disease
 Older age
 Family history of renal disorders
 A previous episode of acute kidney injury
 Kidney donors and transplant rejection
 And presence of- proteinuria, abnormal urinary sediment or structural
abnormalities of the urinary tract
(iii) Patho-physiology-
The kidney is able to adapt to damage by increasing the filtration rate in the remaining
normal nephrons, a process called adaptive hyperfiltration. As a result, the patient with
mild renal injury often has a normal or near-normal creatinine. (2) Additional
homeostatic mechanisms (most frequently occurring within the renal tubules) permit
the serum concentrations of sodium, potassium, calcium, and phosphorous and the
total body water to also remain within the normal range. Physiologic changes observed
in chronic kidney disease-
1 “Uremia.”
2 Almeras and Argilés, “The General Picture of Uremia.”

5.  Increased single nephron GFR
 Afferent arteriolar vasodilation
 Intraglomerular hypertension
 Loss of glomerular perm-selectivity
 Inability to appropriately dilute or concentrate the urine in the face of volume
challenge
 Intraglomerular hypertension and glomerular hypertrophy leading
to glomerular scarring (glomerulosclerosis).
 Additional causes may include systemic hypertension, hyperlipidemia,
metabolic acidosis, and tubule-interstitial disease. Proteinuria typically is
present in patients with progressive CKD, even in primary tubule-interstitial
diseases such as reflux nephropathy.
 Principal targets for renal protection —the blood pressure and proteinuria
maintenance.
 The gradual decline in function in patients with (CKD) is initially asymptomatic.
 However, different signs and symptoms may be observed with advanced RF,
including volume overload, hyperkalemia, metabolic acidosis, hypertension,
anemia, and (MBDs). The onset of (ESRD) results in a constellation of signs and
symptoms referred to as uremia.
(iv) What is CKD?
Chronic kidney disease is defined based on the presence of either kidney damage or
decreased kidney function for 3 or more months, irrespective of cause. Criteria-
 Duration of more than or equal to 3 months, based on documentation or
interference
 GFR < 60 mL/min/ 1.73m2
 Kidney damage defined by structural or functional abnormalities, other than
decreased GFR (3) -
a) Pathologic abnormalities-
-Glomerular diseases: diabetes, autoimmune diseases, systemic
infections, drugs, neoplasia
-Vascular diseases: atherosclerosis, hypertension, ischemia,
vasculitis, thrombotic microangiopathy
3 “Chronic Kidney Disease (CKD).”
Primary insult-
decreased nephron
mass
increased
glomerular volume
and hypertension
Epithelial Cell
Density and Foot
Process Fusion
Glomerular
sclerosis and
hyalinosis

6. -Tubulointerstitial diseases: urinary tract infections, stones,
obstruction, drug toxicity
-Cystic disease: polycystic kidney disease
b) History of kidney transplantation: In addition to pathologic
abnormalities observed in native kidneys, common pathologic
abnormalities include the following:
-Chronic allograft nephropathy: non-specific findings of tubular
atrophy, interstitial fibrosis, vascular and glomerular sclerosis
-Rejection
-Drug toxicity: calcineurin inhibitors
-BK virus nephropathy
-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).*
-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
-Threshold value corresponds approximately to urine dipstick values
of trace or 1+
-High urine ACR can be confirmed by urine albumin excretion in a
timed urine collection.
d) Urine sediment abnormalities as markers of kidney damae:
- RBC casts in proliferative glomerulonephritis
-WBC casts in pyelonephritis or interstitial nephritis
-Oval fat bodies or fatty casts in diseases with proteinuria
-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):
-Polycystic kidneys
-Hydronephrosis due to obstruction
-Cortical scarring due to infarcts, pyelonephritis or vesicoureteral
reflux
-Renal masses or enlarged kidneys due to infiltrative diseases
-Renal artery stenosis
- Small and echogenic kidneys (common in later stages of CKD due to
many parenchymal diseases) (4)
 No direct correlation exists between the absolute serum levels of (BUN) or
creatinine and the development of uremic symptoms for example: some patients
have relatively low levels (eg, a BUN of 60 mg/dL in an older patient) but are
markedly symptomatic; while others have marked elevations (eg, a BUN of 140
mg/dL]) but remain asymptomatic.
 Certain drugs also interfere with either creatinine secretion or the assay used
to measure the serum creatinine for example cimetidine, trimethoprim,
cefoxitin, and flucytosine. In these settings, there will be no change in the true
GFR; Absence of a concurrent elevation in the (BUN). (5)
 Factors contributing to Uremic Syndrome in CKD:
- Toxins
- Homeostasis
4 “What Is Chronic Kidney Disease? | NIDDK.”
5 “Chronic Kidney Disease - Wikipedia.”

7. - Progressive systemic
inflammation
(v) Uremic solutes:
Uremic solutes are classified based
on the sizes:
- Free water solube
molecules e.g. urea
- Middle sized solutes e.g.
beta 2 microglobulin
- Protein bound solutes e.g.
p- cresol acid
3. Clinical abnormalities in Uremia:
Fluid and electrolyte disturbances
Endocrine-metabolic disturbances
Neuromuscular disturbances
Cardiovascular and pulmonary
disturbances
Dermatologic disturbances
Gastrointestinal disturbances
Hematologic and immunologic disturbances
What is Residual Syndrome? (6)
(i) Fluid and electrolyte disturbances
a) Hyponatremia:
- Caused by water restriction
- ECFV expansion – salt restriction
- Thiazides – limited utility in stages 3-5 CKD
- Loop diuretics needed, resistance – Higher doses
- Metolazone –plus loop diuretics, inhibit the NaCl co-transporter of the DCT, can
help effect renal salt excretion
b) Hyperkalemia:
- Seen in both acute and chronic kidney disease, medical emergency if serum
potassium levels cross more than 6.5 mg/dL
- Precipitated by: increased dietary potassium intake, protein catabolism,
hemolysis, hemorrhage, transfusion of stored red blood cells, and metabolic
acidosis or Medications.
- Common cause for initiation of RRT is that thereis limited potassium excretion
as GFR falls
- Diabetics may develop type IV RTA (hyporenemic hypoaldosteronism)
- Use of ACEi can exacerbate hyperkalemia
- Potassium balance usually remains intact until GFR < 10-20 mL/min
- Treatment of acute hyperkalemia involves cardiac monitoring, IV calcium
chloride or gluconate, insulin with glucose, bicarbonate, and potassium-binding
resins
- Chronic hyperkalemia treatment with dietary potassium restriction, and Ca
resonium PRN
c) Hypokalemia:
- Not common in CKD
6 “Table 1 . Uremic Toxins Classification and Characteristics.”

8. - Precipitated by- reduced dietary potassium intake, GI losses, Diuretic therapy,
Fanconi’s syndrome, RTA, Hereditary or acquired Tubulointerstitial disease
d) Metabolic acidosis:
- Metabolic acidosis is a major complication of uremia and ESRD because RTC
are prime regulators of acid- base homeostasis in the kidneys. Due to kidney
failure there is a decreased secretion H+ ions and inability to excrete ammonia
which leads to phosphate and organic acids e.g. lactic acid, sulfuric acid,
hippuric acid build up which leads to increase in the anion gap .
- Symptoms: hyperventilation, lethargy, anorexia, muscle weakness, and
congestive heart failure (due to a decreased cardiac response).
- 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(7)
(ii) Endocrine- metabolic disturbances:
- Secondary hyperparathyroidism
- Adynamic bone
- Vitamin D- deficient osteomalacia
- Carbohydrate resistance
- Hyperuricemia
- Hypertriglyceridemia
- Decreased HDL level
- Protein energy malnutrition
- Impaired growth and development
- Infertility, amenorrhea, sexual dysfunction
- Beta 2 microglobulin associated amyloidosis
- Glucose tolerance, elevated circulating insulin levels
a) Thyroid dysfunction:
- Kidney plays an important role in degradation excretion of various thyroid
hormones and thus, in the case of chronic kidney failure, a thorough
interpretation of tests is needed as the symptoms of uremic syndrome and
hypothyroidism overlap.
- Disturbances: low serum free and total T3, normal rT3 and T4 and TSH levels.
Mostly patients are euthyroid.
b) Calcium and Phosphate metabolism disorder:
- Hypocalcemia occurs due to decreased production of active vitamin D (1,25
dihydroxyvitamin D) which is responsible for gastrointestinal (GI) absorption of
calcium and phosphorus and suppression of parathyroid hormone excretion.
- Hyperphosphatemia occurs because of impaired phosphate excretion in the
setting of renal failure.
- leads to an increase in PTH secretion, Levels of 25-OH D should be measured
when PTH-Intact >70pg/ml
- Recommended Treatment: <5ng/ml 50,000U Ergocalciferol/wk x12, then q
mo x6 5-15ng/ml 50,000/wk x 4, then q mo x 6 16-30ng/ml 50,000/month
x 6, Measure 25(OH)-D at 6 months and Maintenance 800-1200 IU qd.
7 Alcázar Arroyo, “[Electrolyte and acid-base balance disorders in advanced chronic kidney disease].”

9. - The principal complications of abnormalities of calcium and phosphate
metabolism in CKD: occur in the skeleton and the vascular bed, 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,
Tertiary hyperparathyroidism, Renal osteodystrophy: Demineralization, Bone
pain, Fractures, Systemic toxicity: Cutaneous – Calciphylaxis, Cardiovascular,
accelerated vascular calcification.
- Can be treated with calcimemetics for elevated parathyroid levels and vitamin
D sterols for when 25(OH)-D < 30pg/ml and PTH > target and control of
dietary phosphorus intake to 0.8-1g/d May need initiation of “Phosphate
binders” with meals. (8)
(iii) Neuromuscular disturbances-
- Fatigue
- Lethargy
- Sleep disorder
- Headache
- Impaired mentation
- Asterixis
- Muscular irritability
- Restless leg syndrome
- Myoclonus
- Peripheral neuropathy
- Myopathy
- Muscle cramps
- Sezures
- Coma
- Dialysis disequilibrium syndrome (9)
(iv) Cardiovascular and Pulmonary disturbances:
- hypertension: causes increased myocardial oxygen demand
- Accelerated atherosclerosis
- coronary artery disease
- Pericarditis: secondary to retention of metabolic toxins, symptoms may
include a pericardial friction rub, pulsusparadoxus, fever, CP. It is an absolute
indication for initiation of hemodialysis. ECG changes are uncommon as
uremia is not responsible for epicardial changes and thus, may incdicate
another underlying disease.
- pulmonary edema
- Hypotension
- Arrhythmia
8 Slatopolsky, Brown, and Dusso, “Calcium, Phosphorus and Vitamin D Disorders in Uremia.”
9 “Uremic Neuropathy: An Overview of the Current Literature - PubMed.”

10. - Uremic lungs: Kussaumal breathing, decreased cough reflex, dyspnea,
pulmonary edema, uremic pleuritis, pleural effusion, predisposition to
respiratory infections
- Valvular calcifications
- Hypertrophic or dilated cardiomyopathy: LVH in *0% cases
- Heart failure: high outputheart failure, extracellular fluid overload, shunting of
blood through AV fistula, for dialysis and anemia
- Ischemic vascular disease: caused due to anemia, hyperphosphatemia,
hyperparathyroidism, sleep apnea, and generalized inflammation. Cardiac
troponin levels are frequently elevated in CKD without evidence of acute
ischemia.
- Treatment is with Loop diuretics, ACEi and salt and water restrictions (10)
(v) Dermatological disturbances:
- Pallor of oral mucosa secondary to anemia due to decreased erythropoietin
production
- Hyperpigmentation
- Pruritus
- Ecchymoses
- .Nephrogenic fibrosing dermopathy
- Uremic frost: white plaque on the skin or in the mouth, caused by residual
urea crystals left on the epithelial surface after perspiration and saliva
evaporation or as a result of reduced salivary flow. (11)
(vi) Gastrointestinal disturbances:
- Gingivitis, decreased salivary flow, xerostomia, parotitis, ammonia breath also
known as uremic fetor
- Uremic stomatitis: a pseudo- membrane or the frank ulcerations with redness
and a pultaceous coat
- Enamel hypoplasia and tooth erosions in pediatric patients
- Anorexia
- Nausea and vomiting
- Gastroenteritis
- Peptic ulcer
- Gastrointestinal bleeding
- Peritonitis
- Idiopathic ascites: Ascites in ESKD patients is predominantly of the low SAAG
and high protein variety which is a manifestation of the combined effect of
altered peritoneal membrane permeability, fluid overload and under-dialysis.
10 Rehman et al., “Uremic Pericarditis, Pericardial Effusion, and Constrictive Pericarditis in End-Stage Renal
Disease.”
11 “Dermatologic Manifestations of Renal Disease: Overview, Dermatologic Manifestations of Diseases
Associated With ESRD, Dermatologic Manifestations of Uremia.”

11. The severity of ascites is affected by the presence of concomitant cardiac
failure and hypoalbuminemia. (12)
(vii) Hematological and Immunological disturbances-
- Anemia
- Lymphocytopenia
- Bleeding diathesis
- Increased susceptibility to infection
- Leukopenia
- Thrombocytopenia: caused ecchymosis, petechiae and hemorrhages in oral
mucosa
a) Anemia: A normocytic, normochromic anemia develops when the GFR
decreases to < 30-35 ml/min :decreasing production of erythropoietin,
reduced renal mass, uremic inhibition of bone marrow, decreased RBC life-
span, PTH induced marrow fibrosis, Iron deficiency, Folate or vitamin B12
deficiency or Aluminum related bone disease. Investigations: Nonrenal
causes of anemia, Red blood cell indices, Absolute reticulocyte count,
Serum iron, total iron- binding capacity, percent Transferrin saturation,
serum ferritin, White blood cell count and differential, platelet count, B12
and folate if (MCV) is increased, Occult blood in stool. This work-up should
be performed prior to administering ESA therapy.
b) Abnormal hemostasis: prolonged bleeding time, decreased activity of
platelet factor III, abnormal platelet aggregation and adhesiveness, and
impaired prothrombin consumption. Clinical manifestations include: an
increased tendency to bleeding and bruising, prolonged bleeding from
surgical incisions, menorrhagia, and spontaneous GI bleeding
c) Malnutrition: common in patients with advanced CKD because of a lower
food intake (principally due to anorexia), decreased intestinal absorption
and digestion, and metabolic acidosis. Many additional studies have shown
a strong correlation between malnutrition and death in maintenance
dialysis patients. To best assess nutritional status, the serum albumin and
BW should be measured serially; these should be measured approximately
every one to three months and more frequently, if necessary.
d) Infection and Vaccination: Patients with CKD are at increased risk for
infection. The risk of bacterial infection (particularly pulmonary and
genitourinary) increases with the decline in kidney function. Preventive
measures such as influenza and pneumococcal immunization. (13)
(viii) What is Residual Syndrome?
- Toxic effects of metabolites in blood causing the same signs and symptoms of
that of uremia
- Causes:
a) Accummalation of: large molecular weight solutes that are difficultto remove
by dialysis or protein-bound small molecular weight solutes that are difficult to
remove by dialysis or dialyzable solutes that are incompletely removed.
b) Indirect phenomena: Accelerated protein “aging”, Inflammation, Tissue
calcification, Toxic effect of hormone imbalance.
c) A toxic effect of the dialysis itself. (14)
12 Kang, “The Gastrointestinal Tract in Uremia.”
13 Zachée, Vermylen, and Boogaerts, “Hematologic Aspects of End-Stage Renal Failure.”
14 Shemin et al., “Residual Renal Function and Mortality Risk in Hemodialysis Patients.”

12. 4, Diagnosis:
 Diasnosis of renal failure is based on GFR or creatinine clearance.
 Can be performed using 24 hour urine collection or with a a nuclear medicine radioisotope
(iothalamate) clearance assay
 Patients presenting with chronic kidney disease are staged based on the estimated GFR
(creatinine clearance) as calculated by the Modification of Dietin Renal Disease formula by
NKF:
- Stage 1 – normal GFR (90 mL/min or greater)
- Stage 2 – mildly reduced GFR (60 mL/min to 90 mL/min)
- Stage 3 – moderately reduced GFR (30 mL/min to 59 mL/min)
- Stage 4 – severely reduced GFR (15 mL/min to -29 mL/min)
- Stage 5 – ESRD (GFR < 15 mL/min or patient is on dialysis)
 Renal ultrasound to rule out structural abnormalities, and measure the size and shape.
 Brain CT for uremic patients with BUN greater 150 mg/dL to 200 mg/dL are also at an
increased risk of developing spontaneoussubdural hematomas. Abdominal CT is indicative
in doubt of hydronephrosis, if identified on ultrasound.
 MRI for RAS or thrombus or AAA or renal artery dissection, all reversible causes of renal
failure.
 Renal biopsy: for accurate diagnosis in AKI or CKD, helpful in determining reversible and
treatable causes of renal injury. (15)
5. Treatment
 Emergent dialysis is indicated in patients with symptomatic uremia: nausea, vomiting,
hyperkalemia, metabolic acidosis, symptomatic pericardial effusion, or uremic
encephalopathy and should be initiated gently to avoid DDS secondary to cerebral edema
which occurs after initiating dialysis.
 Best treatment is Renal Transplant, even though the primary management constitutes of
hemodialysis and peritoneal dialysis. It improves survival and quality of life.
 Iron replacement for anemia of chronic disease and iron deficiency (as long as serum
ferritin is greater than 100 mcg/mL). Use of erythopoetic stimulants such as erythropoietin
or darbepoetin, can be used additionally in low doses forwhen hemoglobin is below 10g/dL
 Calcium and phosphate metabolism disorders can be managed with oral calcium
carbonate or calcium acetate, oral vitamin D therapy, and oral phosphate binders (e.g.,
calcium carbonate, calcium acetate, sevelamer or lanthanum carbonate).
 Patients with creatinine clearance less than 20ml/min should use loop diuretics, ACEi, ARB,
BB and NSAIDs with caution and should avoid potassium intake.
 ESRD patients are susceptible to bleeding and hemorrhage as uremic toxins buildup, thus
caution should be maintained with the use of anticoagulants or antiplatelet medications.
 Drugs like NSAIDs, aminoglycosides should be avoided as they are renal toxic. Use of N-
acetylcysteine prior to giving IV contrast for radiological imaging might be necessary to
prevent acute kidney injury.
 A diet, with decreased potassium, phosphate and sodium is considered. (16)
15 “Uremia - an Overview | ScienceDirect Topics.”
16 “Uremia Treatment & Management.”

13. 6. Conclusion:
Chronic Kidney disease as the name suggests is a chronic illnesswhich can have potentially
fatal outcomes. And development of uremia may lead to death from kidney failure if not
treated. As, mentioned above the best treatment for chronic kidney failure is renal
transplant but the waiting list for it can take up to 2 to 3 years by which the patient can die
of other underlying causes. Patient survival is increased with the use of hemodialysis or
peritoneal dialysis with proper management of kidney failure.
The understanding of uremia is based on the fact that if it developed due to temporary and
treatable condition e.g. blockage in kidneys or an enlarged prostate or kidney failure is
secondary to various organ involvements.
Uremia is a deadly medical condition that usually signalsa chronic illness underneath. The
patient’s survival and quality of life is dependent of their age, overall health, quality of
treatment and cause of uremia, and severity of uremia. The patient can survive the uremia
if he or she begins prompt treatment. If the treatment is delayed for suspected uremia and
to make ensure they receive the managing treatment.
7. References:
1. “Uremia.” In Wikipedia, April 25, 2020.
https://en.wikipedia.org/w/index.php?title=Uremia&oldid=953063377.
2. Almeras, Cyrielle, and Angel Argilés. “The General Picture of Uremia.” Seminars in
Dialysis 22, no. 4 (August 2009): 329–33. https://doi.org/10.1111/j.1525-
139X.2009.00575.x.
3. “Chronic Kidney Disease (CKD).” Accessed May 21, 2020.
http://www.kidneyfund.org/kidney-disease/chronic-kidney-disease-ckd/.
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https://www.niddk.nih.gov/health-information/kidney-disease/chronic-kidney-disease-
ckd/what-is-chronic-kidney-disease.
5. “Chronic Kidney Disease - Wikipedia.” Accessed May 21, 2020.
https://en.wikipedia.org/wiki/Chronic_kidney_disease.
6. ResearchGate. “Table 1 . Uremic Toxins Classification and Characteristics.” Accessed
May 21, 2020. https://www.researchgate.net/figure/Uremic-toxins-classification-and-
characteristics_tbl1_319765868.
7. Alcázar Arroyo, R. “[Electrolyte and acid-base balance disorders in advanced chronic
kidney disease].” Nefrologia: Publicacion Oficial DeLa Sociedad Espanola Nefrologia 28
Suppl 3 (2008): 87–93.
8. Slatopolsky, Eduardo, Alex Brown, and Adriana Dusso. “Calcium, Phosphorus and
Vitamin D Disorders in Uremia.” Contributions to Nephrology 149 (2005): 261–71.
https://doi.org/10.1159/000085687.

14. 9. “Uremic Neuropathy: An Overview of the Current Literature - PubMed.” Accessed May
21, 2020.
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https://doi.org/10.1002/clc.22770.
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https://doi.org/10.1007/BF01757345.
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Mortality Risk in Hemodialysis Patients.” American Journal of Kidney Diseases: The
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https://doi.org/10.1053/ajkd.2001.25198.
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https://www.sciencedirect.com/topics/medicine-and-dentistry/uremia.
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Hyperkalemia,” November 11, 2019.
https://emedicine.medscape.com/article/245296-treatment.