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12 Metabolic Diseases
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Fig. 12.16 Mass of the lower lip. A mass (arrowhead) is
seen in the mucosa of the lower lip
conrmed to be amyloidosis, the patient should
be referred to a medical clinic even if the clinical
symptoms related to the oral cavity are mild. This
is because oral lesions may lead to the diagnosis
of malignant diseases such as multiple myeloma.
From this point of view, clinical knowledge of
amyloidosis is essential for dentists.
References
1. The Japan Diabetes Society, editor. Guidebook
for diabetes treatment (Tonyobyo Chiryo Guide)
2022–2023 ed. Tokyo: Bunkodo; 2022. p. 14. (in
Japanese).
2. Seino, Y., Nanjo, K., Tajima, N. et al. Report of the
Committee on the classication and diagnostic criteria of diabetes mellitus. Diabetol Int 1, 2–20 (2010).
3. The Japan Diabetes Society, editor. Guidebook for
diabetes treatment (Tonyobyo Chiryo guide). 2022–
2023 ed. Tokyo: Bunkodo; 2022. p. 18. (in Japanese).
4. The Japan Diabetes Society, editor. Guidebook for
diabetes treatment (Tonyobyo Chiryo Guide). 2022–
2023 ed. Tokyo: Bunkodo; 2022. p. 15. (in Japanese).
5. The Japan Diabetes Society, editor. Guidebook for
diabetes treatment (Tonyobyo Chiryo Guide). 20162017 ed. Tokyo: Bunkodo; 2020. p. 8.
6. The Japan Diabetes Society, editor. Guidebook for
diabetes treatment (Tonyobyo Chiryo Guide). 2022–
2023 ed. Tokyo: Bunkodo; 2022. p. 87. (in Japanese).
7. The Japan Diabetes Society, editor. Guidebook for
diabetes treatment (Tonyobyo Chiryo Guide). 2022–
2023 ed. Tokyo: Bunkodo; 2022. p. 92. (in Japanese).
8. The Japan Diabetes Society, editor. Guidebook
for diabetes treatment (Tonyobyo Chiryo Guide).
2022–2023 ed. Tokyo: Bunkodo; 2022. p.94–95. (in
Japanese).
9. Goto A, etal. Diabetes and cancer risk: a Mendelian
randomization study. Int J Cancer. 2019;146(3):712–9.
237
10. The Japan Diabetes Society, editor. Guidebook for
diabetes treatment 2016–2017. Tokyo: Bunkodo;
2016. p.14.
11. The Japan Diabetes Society, editor. Guidebook for
diabetes treatment 2016–2017. Tokyo: Bunkodo;
2016. p.53.
12. The Japan Diabetes Society, editor. Guidebook
for diabetes treatment (Tonyobyo Chiryo Guide).
2022–2023 ed. Tokyo: Bunkodo; 2022. p.49–50 (in
Japanese).
13. The Japan Diabetes Society, editor. Food exchange
lists-dietary guidance for persons with diabetes. 7th
ed. Tokyo: Bunkodo; 2017.
14. Committee for the review of diagnostic criteria
for metabolic syndrome. J Jpn Soc Intern Med.
2005;94:794–809. (in Japanese).
15. Furuya H ed. Shika Masuigaku (Dental
Anesthesiology). 5th ed. Tokyo; Ishiyaku Syuppan. P.
189, 221. 1997. (in Japanese)
16. The Japan Diabetes Society, editor. Japanese clinical
practice guideline for diabetes (Tonyobyo Shindan
guideline). 2016 ed. Tokyo: Nanko-do; 2016. p.293.
(in Japanese).
17. Preshaw PM, etal. Periodontitis and diabetes: a twoway relationship. Diabetologia. 2012;55(1):21–31.
18. The Japan Diabetes Society, editor. Guidebook
for diabetes treatment (Tonyobyo Chiryo Guide).
2020–2021 ed. Tokyo: Bunkodo; 2020. p. 95–6. (in
Japanese).
19. Editorial Board for “Dental Treatment for Patients
with Diseases”, editor. Dental treatment for patients
with diseases: advice to dentistry (Byoukiwo Motta
Kanjyano Shikachiryou: Ika kara Shika heno advice).
Revised ed. Nagasaki: Nagasaki Doctor & Dentist
Association; 2017. p.150–1. (in Japanese).
20. Japan Atherosclerosis Society. Clinical practice
guidelines on dyslipidemia for prevention of arteriosclerotic disease (Doumyakukoukasei Shikkannyobou
notameno Shishitsuijyousho Shinryo guide). 2018th
ed. Tokyo: Japan Atherosclerosis Society; 2018.
p.4–10. (in Japanese).
21. Ministry of Health, Labour and Welfare Japan.
Outline of Vital Statistics in Japan. Table 6: ranking of causes of death per sex and death rates (per
100,000 population). 2017. https://www.mhlw.go.jp/
toukei/saikin/hw/jinkou/kakutei17/dl/10_h6.pdf (in
Japanese). Accessed 22 Feb 2022.
22. Ross R.Atherosclerosis—an inammatory disease. N
Engl J Med. 1999;340(2):115–26.
23. Danesh J, et al. C-reactive protein and other circulating markers of inammation in the prediction of coronary heart disease. N Engl J Med.
2004;350(14):1387–97.
24. Nakajima T, et al. Periodontitis-associated upregulation of systemic inammatory mediator level
may increase the risk of coronary heart disease. J
Periodontal Res. 2010;45(1):116–22.
25. Noack B, et al. Periodontal infections contribute to elevated systemic C-reactive. J Periodontol.
2001;72(9):1221–7.
238
https://t.me/medicina_free
K. Aoki et al.
26. Tonetti MS, etal. Treatment of periodontitis and endothelial function. N Engl J Med. 2007;356(9):911–20.
27. Gordon DJ, Rifkind BM.High-density lipoprotein—
the clinical implications of recent studies. N Engl J
Med. 1989;321(19):1311–6.
28. Kudo C, et al. Analysis of the relationship between
periodontal disease and atherosclerosis within a local
clinical system: a cross-sectional observational pilot
study. Odontology. 2015;103(3):314–21.
29. D’Aiuto F, etal. Periodontal infections cause changes
in traditional and novel cardiovascular risk factors:
results from a randomized controlled clinical trial.
Am Heart J. 2006;151(5):977–84.
30. Lockhart PB, et al. Periodontal disease and atherosclerotic vascular disease: does the evidence support
an independent association? The evidence support
an independent association? : A scientic statement
from the American Heart Association. Circulation.
2012;125(20):2520–444.
31. The Committee for Developing Guidelines for
Prevention and Treatment of Osteoporosis, editor.
Guidelines for prevention and treatment of osteoporosis. Tokyo: Life Science Publishing; 2015. (in
Japanese).
32. Sugimoto T, et al. ASAKURA internal medicine
(Naikagaku). 9th ed. Tokyo: Asakura Shoten; 2007.
(in Japanese).
33. Nishida J, etal. Internal medicine for the odontology
(Shikanotameno Naikagaku). Revised 4th ed. Tokyo:
Nankodo; 2018. (in Japanese).
34. Japanese Society of Oral Implantology, editor.
Treatment guidelines for oral implants 2020 (Koukuu
implant Chiryoushishin 2020 Kensahou Shindan kara
risk management made). Tokyo: Ishiyaku Shuppan;
2020. (in Japanese).
35. Japanese Allied Committee on Osteonecrosis of the
Jaw, Yoneda T, et al. Antiresorptive agent-related
osteonecrosis of the jaw: position paper 2017 of the
Japanese Allied Committee on Osteonecrosis of the
Jaw. J Bone Miner Metab. 2017;35:6–19.
36. Amyloidosis Research Group, Health and Labor
Sciences Research Grants, Research Project for
Overcoming Intractable Diseases. Guidelines for the
treatment of amyloidosis 2010. (in Japanese). http://
amyloidosis- research- committee.jp/wp- content/
uploads/2018/02/guideline2010.pdf. Accessed 22 Feb
2022.
37. Sanchorawala V, etal. Long-term outcome of patients
with AL amyloidosis treated with high-dose melphalan and stem cell transplantation: a 20-year experience. Blood. 2015;126:2345–7.
38. Jaccard A, etal. High-dose melphalan versus melphalan plus dexamethasone for AL amyloidosis. N Engl J
Med. 2007;357:1083–93.
39. Benson MD, et al. Amyloid nomenclature 2018:
recommendations by the International Society
of Amyloidosis (ISA) nomenclature committee.
Amyloid. 2018;25(4):215–9.
40. Fijita T, Idou S, etal. A case of amyloidosis with multiple myeloma accompanied by rapidly growing macroglossia (Kyusokuni Zoudaishi Kyozetsuwo Teishita
Tahatsusei Kotsuzuisyu nitomonau Amylodosis no
Ichirei). Jpn J Oral Maxillofac Surg. 2014;61:25–30.
(in Japanese).
41. Kawamata A, Yamada T, etal. A case report of localized nodular amyloidosis of the sublingual gland.
(Zekkasenni Hasseishita Kyokugensei Kessetussei
Amylodosis no Ichirei.). Jpn J Oral Maxillofac Surg.
2013;59:38–42. (in Japanese).
42. Shibata A, Shimizu T, et al. A case of bilateral primary localized amyloidosis of the angle of the mouth
(Ryougawa Koukakuni Hassyoushita Genpatsusei
Kyokugensei Amylodosis no Ichirei). Jpn J Oral
Maxillofac Surg. 2012;58:252–6. (in Japanese).
43. Yamashiro T, Nakamatsu K, etal. A case of amyloidosis with massive hematoma of the lower lip and the
buccal mucosa (Kashinto Hoonenmakuni Kouhanna
Kessyuwo Keiseisita Amylodosis no Ichirei). Jpn J
Oral Maxillofac Surg. 2010;56:705–9. (in Japanese).
44. Kimura Y, Shimahara M, et al. A case of systemic
amyloidosis with swelling in the tongue and submandibular region as an initial symptom (Zetsu oyobi
Gakukabu no Shucyou wokeikini Hakkennsareta
Zenshinsei Amylodosis no Ichirei). Jpn J Oral
Maxillofac Surg. 2009;55:71–5. (in Japanese).
45. Brenes-salazar JA, Grogan M, et al. A 66-year-old
woman with an enlarged tongue. Cleve Clin J Med.
2013;80(11):696–7.
46. Liakou CI, Koh J, etal. A tongue lesion as a sign of a
systemic disease. Case Rep Med. 2016;2016:6723575.
https://doi.org/10.1155/2016/6723575.
47. Nakasone T, Matayoshi A, etal. A case of massive
macroglossia caused by senile systemic amyloidosis
(Roujinsei Zenshinsei amyloidosis niyori Shoujita
Kyozetsusyou no ichirei). Jpn J Oral Maxillofac Surg.
2016;62:304–8. (in Japanese).
48. Japanese Society of Nephrology, editor. Evidence ni
Motozuku CKD Shinryo guideline 2018 (Evidencebased clinical practice guideline for CKD 2018).
Tokyo: Tokyo Igaku-sha; 2018. (in Japanese).
Kidney Diseases
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MasanoriTokumoto, KoichiHayashi,
HiroshigeOhashi, andAkiraSasaki
13
1 Nephritis [1–3]
MasanoriTokumoto
Nephritis can be divided into glomerulonephritis
and interstitial nephritis according to the site of
inammation in the kidney, and acute and
chronic nephritis according to the degree of progression. In this section, acute glomerulonephritis, rapidly progressive glomerulonephritis,
chronic glomerulonephritis, and acute interstitial
nephritis, which are not partial diseases of systemic diseases but primary and relatively frequent diseases, are reviewed.
M. Tokumoto (*)
Department of Nephrology, Japanese Red Cross
Fukuoka Hospital, Fukuoka, Japan
e-mail: m-tokumoto@fukuoka-med.jrc.or.jp
K. Hayashi
Department of Emergency and Critical Care
Medicine, St. Marianna University Yokohama Seibu
Hospital, Yokohama, Kanagawa, Japan
H. Ohashi
Asahi University Hospital, Gifu, Japan
A. Sasaki
Okayama University, Okayama, Japan
Department of Dentistry (Oral Surgery), Kurashiki
Central Hospital, Kurashiki, Okayama, Japan
1.1 Acute Glomerulonephritis
1.1.1 Denition
It is a syndrome of acute onset of hematuria, proteinuria, decreased glomerular ltration rate
(GFR), sodium (Na)/water retention, and
hypertension.
1.1.2 Pathophysiology
It develops after an incubation period of
1–2 weeks following upper respiratory tract
infection. Some of the infectious pathogens
become antigens, forming immune complexes
and depositing them in the glomeruli, and inammatory cells accumulate and endothelial cells
and mesangial cells proliferate, resulting in
obstruction of blood vessels in the glomeruli and
impairment of glomerularblood ow. As a result,
GFR and urine volume decreases, and sodium
and water accumulate, causing hypertension and
edema. Typically after hemolytic streptococcal
(streptococcal) infection; conventionally, about
80–90% of cases were group A beta-hemolytic
streptococcus, and streptococcus pneumoniae,
staphylococcus aureus, fungi, and parvoviruses
have been reported as causative pathogens in
recent years.
1.1.3 Epidemiology
It is common in children and adolescents, but
also occurs in the elderly.
© The Author(s), under exclusive license to Springer Nature Singapore Pte Ltd. 2023
T. Chiba, H. Yamada (eds.), Internal Medicine for Dental Treatments,
https://doi.org/10.1007/978-981-99-3296-2_13
239
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1.1.4 Symptoms
Hematuria, edema, and hypertension are the
main symptoms. Gross hematuria (brown or
cola color) is observed in about one third of
cases, but it disappears in a few days to 2weeks.
Edema is present on the face and upper and
lower extremities, and is more pronounced
around the eyelids on waking. The patient may
have oliguria with urine volume of less than
400mL/day, and excessive circulating plasma
volume may cause symptoms of heart failure.
1.1.5 Clinical Examination
Microscopic hematuria is always present, and most
cases are accompanied by erythrocyte cast and proteinuria. Blood tests show a decrease in complements (CH50, C3) early in the course of the disease
and an increase in serum antibody titers such as
antistreptolysin O (ASO) and antistreptokinase
(ASK) if after streptococcal infection. Bacteria
may be detected in pharyngeal culture. GFR is
decreased in about half of cases, and blood urea
nitrogen (BUN) and serum creatinine (Cr) may be
transiently elevated. Renal biopsy shows many
inammatory cells, including neutrophils lling
the vascular lumen, such as endocapillary proliferation, and immunouorescence microscopy shows
granular deposition of C3 along the glomerular
capillary wall and granular deposition of IgG in the
early stages of the disease.
1.1.6 Treatment
Rest and diet therapy (high calorieintake, protein
and salt restriction) are main, and rest in the early
stages of illness is particularly important. If
streptococcal infection is conrmed in the early
stages of illness, antibacterial agents such as penicillin may be used, but not if the infection has
been already cured. If hypertension and edema
cannot be treated by salt restriction, diuretics
should be administered. Antihypertensive agents
may also be used to treat hypertension.
1.1.7 Prognosis
In children, more than 90% of cases are completely
cured within 3–6months, but the cure rate decreases
with age, and the cure rate in adults is about
60–80% and the disease tends to become chronic.
1.2 Rapidly Progressive
Glomerulonephritis
1.2.1 Denition
It is a syndrome of rapidly progressive renal failure over a period of weeks to months, accompanied by urinary abnormalities indicative of
nephritis.
1.2.2 Pathophysiology
More than half of the cases have systemic vasculitis
with positive of antineutrophil cytoplasmic antibodies (ANCA) in the blood, but acute glomerulonephritis, other primary glomerulonephritis, and infectious
and collagen diseases may also be the cause.
1.2.3 Epidemiology
It is common in middle-aged and elderly people.
1.2.4 Symptoms
Most of the initial symptoms are non-specic,
such as fever, arthralgia/myalgia, and loss of
appetite. As renal dysfunction progresses, edema,
hypertension, oliguria, and anuria are observed.
Respiratory symptoms are also common.
1.2.5 Clinical Examination
Hematuria, proteinuria, and cylindruria are
observed, and GFR is decreased and BUN and
serum Cr are increased. Inammatory ndings
such as elevated CRP and erythrocyte sedimentation rate, and severe anemia relative to the degree
of renal dysfunction are often observed. ANCA
and anti-glomerular basement membrane (GBM)
antibodies are often positive, and reduced complements are not rare. The typical case is crescentic glomerulonephritis, in which more than 50%
of glomeruli on renal biopsy show the formation
of a crescent (increased epithelial cells of
Bowman’s capsule, monocytes, macrophages,
and other cells that look like a crescent). There
are various types in this disease. It can be divided
into three types by immunouorescence microscopy: (1) immunocomplex type, in which IgG is
deposited in granular pattern on the glomerular
capillary wall and mesangium; (2) anti-GBM
antibody type, in which IgG is deposited in linear
pattern on the glomerular capillary wall; and (3)
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241
pauci-immune type, in which immune complexes
are less deposited. In Japan, pauci-immune type
is the most common, and ANCA is found in many
cases.
1.2.6 Treatment
Immunosuppressive therapy with corticosteroids
and immunosuppressive drugs is the basic treatment. In the initial stage, oral corticosteroids are
administered, and high-dose intravenous corticosteroids are used when there are severe inammatory ndings or multiple organ involvement.
Immunosuppressive drugs are used in combination depending on the condition of the patient. In
Europe and the United States, plasma exchange
therapy is used for alveolar hemorrhage patients
with ANCA-associated vasculitis or anti-GBM
antibodies.
1.2.7 Prognosis
The renal prognosis and vital prognosis are both
poor, and dialysis is often required, but there are
cases of death during the course.
1.3 Chronic Glomerulonephritis
1.3.1 Denition
It is a primary glomerular disease in which
abnormalities in urinalysis such as proteinuria,
hematuria, and cylindruria persist for more than
1year.
1.3.2 Pathophysiology
It is thought to be caused by an antigen-antibody
reaction in the local glomeruli or by the deposition of immune complexes formed in the blood to
the glomeruli, resulting in an immune reaction in
the local glomeruli. With persistent inammatory
stimulation, glomerular component cells, inltrating leukocytes, and platelets produce growth
factors, proteolytic enzymes, and reactive oxygen
species, resulting in inammation not only in the
glomeruli but also in the interstitium.
Furthermore, hemodynamic changes in the glomerular region cause glomerular hypertension,
which leads to glomerulosclerosis via glomerular
hyperltration.
1.3.3 Epidemiology
It is the second most common primary cause of
dialysis initiation and is more common in young
patients than in the elderly.
1.3.4 Classication
Histopathologically, there are several types of
nephropathy such as IgA nephropathy, mesangial
proliferative glomerulonephritis, membranous
nephropathy, membranoproliferative glomerulonephritis, minimal change nephrotic syndrome,
focal glomerulosclerosis, etc. In Japan, the frequency of IgA nephropathy is the highest.
IgA Nephropathy
1. Outline: This is a mesangial proliferative glomerulonephritis with granular deposition of
IgA in the mesangial region of the glomeruli.
2. Epidemiology: This is the most common primary chronic glomerulonephritis in Japan,
accounting for more than 30% of chronic glomerulonephritis in adults. Because of the lack
of symptoms, it is often detected by abnormal
urine analysis.
3. Symptoms: In most cases, the symptoms are
asymptomatic, but gross hematuria, edema,
and hypertension may be observed with upper
respiratory tract infection.
4. Clinical Examination: Microscopic hematu-
ria is almost always observed, and deformed
erythrocytes or erythrocytic cast may be seen
in the urinary sediment. Proteinuria is also
common. Serum IgA is elevated in more than
half of patients, and renal function may be
impaired at the time of diagnosis. Renal
biopsy shows proliferation of mesangial cells
and enlargement of the mesangial matrix,
which may be accompanied by a crescent.
Immunouorescence microscopy shows granular IgA deposition mainly in the mesangial
region, often accompanied by C3 deposition.
5. Treatment: Dietary therapy (high calo-
rie intake, protein and salt restriction) and
drug therapy are the basic treatments. In the
group with low activity and low possibility of
end-stage renal failure, the patient is observed
without drug therapy. Patients with highly
active acute lesion should be treated with
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M. Tokumoto et al.
corticosteroids. Inhibitors of the reninangiotensin system are often used to inhibit
the increase in intraglomerular pressure and
reduce proteinuria.
6. Prognosis: The prognosis had been thought to
be good with a relatively gradual course, but it
has become clear that approximately 20–40%
of patients progress to end-stage renal failure
and require hemodialysis more than 20years
after diagnosis. In general, the prognosis is
poor in patients with hypertension and high
levels of proteinuria in the early stage of the
disease.
1.4 Acute Tubulointerstitial
Nephritis
1.4.1 Pathophysiology
Allergy to drugs such as antimicrobials, nonsteroidal anti-inammatory agents, diuretics, uric
acid synthesis inhibitors, and anti-ulcer agents is
the main cause of the disease, which develops
more than 2weeks after initiation of the drug. All
drugs are possible causes.
1.4.2 Symptoms
Patients may be asymptomatic and may complain
of anorexia, nausea and vomiting, and general
malaise. They may also complain of back pain
associated with renal enlargement, skin rash
associated with drug allergy, fever, and
arthralgia.
1.4.3 Clinical Examination
Both proteinuria and hematuria are mild, but
tubular injury results in increased urinary excretion of low-molecular-weight proteins (α1 and
β2-microglobulin) that is absorbed from the
tubular epithelium and N-acetylglucosaminidase
(NAG) that is an enzyme in tubular epithelium.
Sterile pyuria is characteristic, and eosinophils
may be detected in the urine. In blood tests, both
BUN and serum Cr are elevated, but the BUN/
Cr ratio is characteristically less than 10. In
drug allergy, there is an increase in peripheral
blood eosinophils and serum IgE. In renal
biopsy, glomeruli are almost normal, and there
is marked inammatory cell inltration and
edema in the interstitium surrounding the
injured tubules.
1.4.4 Treatment andPrognosis
In cases of drug-inducedacute tubulointerstitial
nephritis, renal function often recovers with discontinuation of the causative drug. The prognosis
is good if the disease is detected early, and complete remission is usually achieved. If renal function does not improve after discontinuation of the
causative drug, corticosteroids or immunosuppressive drugs may be administered. Oliguria and
uremia may occur, and hemodialysis may be
required.
2 Acute Renal Failure [4–7]
KoichiHayashi
2.1 Disease Overview
Acute renal failure (ARF) is a life-threatening
condition caused by a rapid decline in renal
function, resulting in accumulation of metabolites, electrolyte abnormalities, disturbance of
acid- base equilibrium, and dysregulation of
uid volume. Until now, there has been no
denitive denition of the diagnosis of acute
renal failure, but much attention has been mainly
focused on the search for the cause and countermeasures against complications, rather than on
early detection. In recent years, the concept of
acute kidney injury (AKI) has been proposed to
improve the prognosis by early diagnosis and
intervention, and the denition of AKI has been
established. The transition in perception from
acute renal failure to AKI is now well
established.
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243
Table 13.1
injury
Stage
1
Stage 2sCr elevated 2.0–2.9
Stage 3sCr elevated>3.0
Denition
1. ΔCr≥0.3mg/dL (within 48h)
2. 1.5 times higher than the reference value of sCr (within
7days)
3. Urine output of 0.5mL/kg/h or less for more than 6h
Note: Diagnosis of AKI is made if one of denitions 1–3
is met; in severity classication by SCr and urine output,
the higher severity is adopted
Diagnostic criteria for stage of acute kidney
sCr criteria
ΔCr≥0.3mg/dL or
1.5–1.9 timessCr
elevated
times
times or sCr>4.0mg/
dL or start of renal
replacement therapy
Urinary
excretioncriteria
0.5mL/kg/h or less for
more than 6h
0.5mL/kg/h or less for
more than 12h
0.5mL/kg/h or less for
more than 24h or
anuria for more than
12h
The RIFLE, AKIN, and KDIGO criteria have
been proposed as denitions of AKI, and in 2016,
Japanese guidelines for the treatment of AKI
have been developed based on the KDIGO criteria. Thus, AKI is dened based on the degree of
increases in serum creatinine levels and changes
in urine volume (Table13.1).
2.2 Pathophysiology
The rapid decline in renal function and urine output is central to the pathophysiology of the disease, but it does not matter whether the primary
cause is renal or extrarenal. It includes not only
direct renal damage such as acute tubular necrosis, nephritis, and vasculitis, but also functional
renal damage such as heart failure, hypotension,
hepatorenal syndrome, and sepsis. Consequently,
decreased glomerular ltration and reduced urine
volume and sodium excretion ensue.
Risk factors for AKI include age, male gender,
pre-existing chronic kidney disease, diabetes
mellitus, and heart failure, as well as sepsis, heart
failure, and cardiac surgery (Table13.2).
Table 13.2
Patient-specic AKI risk
factors
Aging Advanced disease
Male Septicemia
Colored person Cardiac surgery
Preexisting chronic kidney
disease
Albuminuria Acute heart failure
Hypertension Exposure to contrast
Diabetes mellitus Drug toxicity,
Anemia Injury
Complications of chronic liver
disease and portal
hypertension
Heart failure, impairment of
cardiac contractility
Chronic obstructive
pulmonary disease
Peripheral vascular disease
Malignant tumor
Risk factors for acute kidney injury
AKI risk factors
according to the
disease state
Major non-cardiac
surgeries
media
nephrotoxic substances
2.3 Epidemiology
The incidence of AKI has been increasing due to
the aging of the population and the increase in
lifestyle-related diseases. Although there are
some issues such as the difference in data collection, there is a difference in the incidence of AKI
between inpatients and outpatients. In hospitalized patients, the average incidence was 23%,
and the incidence related to intensive care and
cardiac surgery was particularly high, with the
most common causes being renal ischemia, nephrotoxic substances, and sepsis. In contrast, the
incidence of out-of-hospital AKI is higher in lowand middle-income countries, and the proportion
of out-of-hospital AKI is higher in low-income
countries. Factors associated with out-of-hospital
AKI include dehydration, infection, and
childbirth.
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M. Tokumoto et al.
Table 13.3
Mechanism Functional renal
Cause Shock
FENa <1% >1%
FENa (fractional Na excretion) = 100 × (urine Na concentration × serum Cr concentration)/(serum Na concentration×urine Cr concentration). Cr creatinine
Classication of acute kidney injury
Prerenal Renal Postrenal
hypoperfusion
Dehydration
Bleeding
Burns
Postoperative period
Heart failure
Nephrotic syndrome
Renal parenchymal disorder Urinary tract excretion
Glomerular and vascular
disorders
Malignant hypertension
Glomerulonephritis
Renal tubular
impairment
Acute tubular
necrosis
Interstitial
nephritis
disorder
Prostatic hypertrophy
Bilateral ureteral
obstruction
Neurogenic bladder
bilateral ureteral obstruction, or neurogenic blad-
2.4 Categories
der. FENa is elevated (>1%).
AKI is classied into prerenal, renal, and postrenal one according to the mechanism of renal
2.5 Symptoms
involvement (Table13.3). Fractional Na excretion (FENa) indicates sodium reabsorption in the
renal tubules, and the response to AKI varies
depending on the location of the lesion.
Uremic symptoms such as oliguria,
edema, hypertension, cardiac failure, pulmonary congestiondue to uid retention, anorexia,
and nausea may occur. In acute and severe cases,
disturbance of consciousness and convulsion
2.4.1 Prerenal
Prerenal AKI is dened as a condition in which
glomerular ltration is reduced due to a
decrease in renal blood ow. It is caused by
dehydration, hemorrhage, burns, postoperation,
heart failure, nephrotic syndrome, etc. FENa is
low (<1%).
may also occur.
Regarding hyperkalemia and hypocalcemia,
as a result of electrolyte abnormalities, special
attention should be paid to atrioventricular block
and ventricular tachycardia (caused by hyperkalemia), and QT prolongation and ventricular
tachycardia (caused by hypocalcemia).
2.4.2 Renal
Renal parenchymal damage results in decreased
glomerular ltration.
It is caused by glomerulonephritis with primary glomerular lesions, and acute tubular necrosis or acute tubulointerstitial nephritis presenting
mainly tubular lesions.
FENa is low (<1%) in glomerular lesions and
high (>1%) in tubular lesions.
2.4.3 Postrenal
Postrenal AKI is caused by an excretory disorder
of the urinary tract, such as prostatic hypertrophy,
2.6 Laboratory Examination
There is an increase in blood urea nitrogenlevel,
serum levels ofcreatinine, potassium, and phosphorus due to acute renal dysfunction, a decrease
in serumbicarbonate leveldue to metabolic acidosis, and an increase in serum chloride. On the
other hand, serum sodium and calcium tend to
decrease. In general, when renal function is
totally impaired, serum creatinine is elevated by
0.5–1.0 mg/dL per day. Anemia may also be
present.
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2.7 Treatment
In prerenal cases, uid correction or elimination of the cause of functional renal hypoperfusion should be done. In postrenal cases, the
cause of urinary tract obstruction should be
removed. In renal cases, drugs should be discontinued, steroid hormones may be administered, and immunosuppressive therapy should
be used in rapidly progressive
glomerulonephritis.
In all cases, dialysis therapy is indicated if
no improvement is expected. In prerenal and
postrenal cases, renal function may improve
with elimination of the cause. In renal cases,
there is relative improvement if the cause is
drug-induced, but renal dysfunction often
remains in other causes. In both prerenal and
postrenal cases, the disease may progress to
renal paremchymal AKI if appropriate treatment is not given.
Hemodialysis is often selected as dialysis
therapy, but peritoneal dialysis may be used in
cases of circulatory instability or cerebral hemorrhage. In hemodialysis, continuous or intermittent hemodialysis may be chosen depending on
circulatory dynamics.
2.8 Prognosis
When comparing hospital-onset AKI with outof- hospital-onset AKI, in-hospital-onset AKI is
generally associated with a worse prognosis.
Similarly, when septic AKI is compared with
non-septic AKI, mortality is higher in septic
AKI.
In AKI, renal dysfunction develops acutely
but usually recovers, however, it may be irreversible depending on the pathogenesis of the
primary disease. In recent years, a history of
AKI has been recognized as a risk factor for
chronic kidney disease and is considered to be a
risk factor for future chronic kidney disease.
Thus, it isimportant to prevent the development
of AKI.
2.9 Recent Findings
Among urinary biomarkers, urine NGAL and
urine L-FABP may be useful for early diagnosis
of AKI.
peptide and low-dose dopamine in the prevention
and treatment of AKI is not clear. Loop diuretics
are not effective for prophylaxis or treatment, and
their use is not recommended except for the correction of uid overload.
3 Chronic Renal Failure [8–10]
HiroshigeOhashi
3.1 Disease Overview
Chronic renal failure (CRF) is a syndrome in
which the function of the kidneys declines to the
point where they do not recover continuously for
several months to several years or more, regardless of the primary disease, resulting in a variety
of symptoms.
the number of functioning nephronsin CRF.The
remaining nephrons cannot withstand the excessive
load and drop out, further reducing the number of
nephrons and leading to end-stage renal failure.
such as malaise, anorexia, and edema appear,
resulting in uremia. In other words, uremia is an
advanced state of chronic renal failure and is
characterized by the appearance of systemic
symptoms unrelated to the kidney.
3.2 Pathophysiology
Chronic renal failure differs signicantly from
acute renal failure in that it is irreversible with
little chance of recovery.
function in a short period of time, hours or days.
It may be caused by an abnormality in the kidney
The usefulness of low-dose atrial natriuretic
Decreased renal function means a decrease in
In end-stage renal failure, systemic symptoms
Acute renal failure refers to the loss of renal
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M. Tokumoto et al.
itself or by insufcient blood supply to the kidney due to shock, massive bleeding, severe diarrhea, or vomiting. However, acute renal failure is
characterized by rapid healing.
Chronic renal failure (CRF) is a syndrome in
which renal function declines over a chronic
course, independent of the primary disease. It is
important to understand the causes of chronic
renal failure in order to determine treatment and
prognosis.
When the number of nephrons decreases, the
remaining nephrons are further overloaded,
resulting in glomerular hyperltration, which
further decreases the number of nephrons by
hemodynamic mechanisms, decreases glomerular function, and increases creatinine:(Cr) in the
blood.
Once chronic renal failure occurs, regardless
of the primary disease, recovery is unusual and
renal function declines further.
3.3 Epidemiology
It is estimated that there are 50,000–70,000
patients with chronic kidney disease stage 5 in
Japan, and it is necessary to prevent the progression to dialysis and to suppress the development
of complications such as cardiovascular disease
during the course of the disease.
pressure control via the renin-angiotensin system, blood pressure often increases when
renal function declines.
2. Gastrointestinal symptoms: The accumulation
of uremic toxin causes anorexia and
dysgeusia.
3. Renal anemia: Red blood cells are produced
in the bone marrow, but when anemia occurs,
erythropoietin is produced in the kidneys, and
red blood cells are produced in the bone marrow to prevent anemia. Therefore, anemia
appears and progresses when renal function
declines.
4. Metabolic acidosis: Because the kidneys
excrete acidic urine, when renal function is
impaired, the body becomes acidic. The disease is asymptomatic, but hyperkalemia may
occasionally occur.
5. Secondary hyperparathyroidism (osteitis brosa): Calcium (Ca) ingested orally is
absorbed from the intestinal tract. In renal
failure, hyperphosphatemia due to decreased
phosphorus (P) excretion and hypocalcemia
due to impaired vitamin D activation with
reduction of Ca absorption from the intestinal
tract are observed. In order to correct the
hypocalcemia, the parathyroid gland increases
its activity, producing more parathyroid hormone (PTH), mobilizing Ca from bone, and
decreasing bone mineral density.
3.4 Symptoms
Symptoms of renal disease include abnormalities
in urinalysis, such as proteinuriaand hematuria,
changes in urine volume, edema, and elevated
blood pressure; further deterioration of renal
function leads to uremia.
Symptoms of uremia include general malaise,
anorexia, nausea with vomiting, uncontrollable
blood pressure, dyspnea, and sleep disturbance.
1. Cardiovascular symptoms: The accumulation
of sodium (Na) and water may cause heart
failure, and hyperkalemia (K) may cause
arrhythmia. Because the kidneys play an
important role in sodium excretion and blood
3.5 Clinical Examination
3.5.1 Urinalysis
This is the most important test, although it is simple. It is important to conrm whether there are
any abnormalities in the urine sample, whether
proteinuria is present alone or in combination
with hematuria, and whether proteinuria is severe
or not.
In diabetic nephropathy, hematuria is rare and
proteinuria is predominant, and when proteinuria
is accompanied by hematuria, chronic glomerulonephritis is more likely. In nephrosclerosis,
there are often no abnormalities in urinalysis
such as proteinuria or hematuria.
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