Type 2 diabetes Hypothyroidism Acute Renal Failure

Epidemiology  Prevalence for this  Occurs commonly in  Commonly seen in

disease is highest women and elderly (>65 hospitalized or critically ill
among Alaska years), affecting patients (Koza, 2016)
Natives and American approximately 0.1-2% of  Risk factors include: age
Indians at 16%, and the U.S population (elderly), sepsis, undergoing
lowest among non- (McCance et al., 2019) major surgery, exposure to
Hispanic whites at  Associated with iodine nephrotoxic agents (ex:
7.6% (McCance & status – iodine deficient contrast dyes), overuse of
Huether, 2019). populations (Chaker, NSAIDs and obesity (Nie,
 Increased prevalence Bianco, Jonklaas, & Peeters, Tang, Zhang, Feng, &
for type 2 diabetes 2017). Chen, 2017).
mellitus (DM) also  Common among those with  Comorbidities have been
found in obese autoimmune diseases, such found to be a significant
children (McCance et as type 1 diabetes, celiac predictor of acute kidney
al., 2019) disease and gastric atrophy injury (AKI). These include:
 Linked to genetic- (Chaker et al., 2017) -Diabetes
environmental  Increased risk among those -Hypertension
interplay, risk factors with Turners’ syndrome or -Chronic liver disease
most commonly Downs’ syndrome (Chaker -Cardiovascular disease
involved with type 2 et al., 2017). -Chronic obstructive
DM include: Obesity,  Family history of thyroid pulmonary disease (Nie et
increased age, disease or autoimmune al., 2017)
physical inactivity, disease (Chaker et al., 2017)
history of  Of Caucasian or Asian  Abnormal laboratory values
hypertension (HTN), ethnicity (Chaker et al., placing the patient at higher
and family history. 2017) risk for AKI include:
 Western style diet:  Thyroid surgery or hyperglycemia, anemia,
high red meat intake, radioactive treatment for excess of uric acid in the
processed foods, high hyperthyroidism (McCance blood and hypoalbuminemia
 fat and sugar content, et al., 2019) (Nie et al., 2017)
pre-packaged foods,  Vitamin D deficiency,  Mixed reviews were found
fried foods (Kolb & selenium deficiency on the risk factors for AKI
Martin, 2017).  Moderate alcohol intake associated with different
 Smoking, short sleep (Chaker et al., 2017) genders and ethnicities.
duration, sedentary
lifestyle, occupations ***Note: AKI can be broken down
involving long into three categories depending on
durations in traffic the injury of which cause the illness
(ex: truck driver) or (McCance et al., 2019).
sitting, increased 1) Prerenal AKI (renal
stress and depression hypoperfusion)
(Kolb et al., 2017) 2) Intrarenal AKI (involving
 Linked to low renal parenchyma and
socioeconomic tissues)
position (Kolb et al., 3) Postrenal (acute urinary
2017) tract obstruction)
Time course  Potentially reversible  Presents gradually over a  This illness presents as an
in early stages, this span of months to years acute, sudden decline in
disease presents as (McCance et al., 2019). kidney function (McCance
chronic, progressing  This condition continues to et al., 2019)
over time. (McCance worsen if left untreated  Minimal to severe, this
et al., 2019)  Consistent management condition worsens, and if
 With a consistent diet through drug therapy can left untreated can be fatal
and exercise routine, stabilize this disease (McCance et al., 2019)
this illness can remain (Chaker et al., 2017)  This illness can be
stable. The illness considered episodic due to
worsens if it is poorly the sudden appearance of
maintained or left symptoms, which are then
untreated (McCance broken down into 4 phases,
 et al., 2019). ending with the recovery
phase (McCance et al.,
2019)
Signs and Symptoms Signs and symptoms of type MOST COMMON signs and Signs and symptoms of AKI
2 DM include: symptoms of hypothyroidism in include: (early manifestations)
 Fatigue, adults include:  Fluid retention / edema
pruritis/itching, visual  Lethargy/fatigue  Nausea/vomiting
changes, weakness,  Cold intolerance  Fatigue
paresthesia, recurrent  Weight gain  Uremia
infections, poor  Dry skin  Delayed wound healing
wound healing  Constipation  Oliguria
(McCance et al.,  Changes in voice  Pruritis
2019) ***Symptoms differ depending on (McCance et al., 2019)
 Patient may present sex, age, and the timeline between
with a history of onset and diagnosis*** Laboratory findings include:
HTN, elevated  Increased serum creatinine
cholesterol, obesity, Elderly patients often present with  Increase blood urea nitrogen
and/or fewer and less “classic” symptoms  Hyperkalemia
hyperinsulinemia of hypothyroidism (Chaker et al.,
(McCance et al.,  Hyperphosphatemia
2017)  Casts noted on urinalysis
2019)
 Symptoms of frequent  Hematuria
Signs / symptoms found in
urination and extreme  Proteinuria
advanced, untreated
thirst may be present (Koza, 2016)
hypothyroidism include:
(McCance et al.,  Goiter
2019) The progression of AKI is placed
 Confusion / memory loss into four categories:
 Decreased cardiac output 1)Initiation phase
 Enlarged heart 2)Extension phase
 Hypoventilation / carbon 3)Maintenance phase
dioxide retention 4)Recovery phase

Pathophysiology Obesity is one of the main
factors in the development of
type 2 DM due to it’s
involvement in insulin
resistance (McCance et al.,
2019). Adipokines, including
adiponectin and leptin, are
hormones that are found in
body fat: In obesity,
adiponectin is decreased,
while leptin is increased. This
causes inflammation,
resulting in decreased insulin
synthesis (McCance et al.,
2019). Additionally,
lipotoxicity occurs from
intracellular deposits of
cholesterol and triglycerides,
and increased levels of free
 Decreased kidney function
 Fluid retention/edema
 Myxedema
 Hypothermia
 Bradycardia
 Dyspnea
 Anemia (Chaker et al.,
2017)
In hypothyroidism, primary
hypothyroidism accounts for
majority of all cases. This is most
commonly caused by autoimmune
thyroiditis (Hashimoto disease),
which consists of continual
inflammatory destruction of thyroid
tissue. High concentrations of
thyroid peroxidase antibodies as
well as anti-thyroglobulin
antibodies are found in these
patients (Chaker et al., 2017) Loss
of thyroid function through this
mechanism results in a decreased
production of thyroid hormone
(TH), in turn increasing the
secretion of thyroid stimulating
hormone (TSH) and thyroid
releasing hormone (TRH)
(McCance et al., 2019)
***Symptoms of AKI may differ
depending on which phase the
patient is in.
 Urine output is lowest
during the maintenance
phase
 Diuresis is common during
the recovery phase
AKI often occurs due to decreased
renal blood flow, extracellular
volume depletion or inflammatory
destruction to kidney cells
(McCance et al. 2019). This causes
variations in renal function that
range from mild to severe.
-In Prerenal AKI, injury results
from inadequate kidney perfusion,
caused by hypotension,
hypovolemia, sepsis, renal
vasoconstriction, artery stenosis,
kidney edema, decreased cardiac
output and multiple organ
dysfunction (McCance et al., 2019).
During the early phases of
hypoperfusion, the glomerular
filtration rate (GFR) is supported
fatty acids (FFA’s).
Inflammatory cytokines are
also released due to obesity –
caused by adipocyte-
associated mononuclear cells
and activated macrophages
(McCance et al., 2019).
In type 2 DM, several
mechanisms contribute to
insulin resistance including:
 Increased amounts of
insulin antagonists
 Abnormality of
insulin molecule
 Decreased activation
of post-receptor
kinases
 Suppressed insulin
receptors
 Changes to glucose
transporter proteins
(GLUT) (McCance et
al., 2019)
Hyperinsulinemia acts as the
body’s compensatory
mechanism, keeping the
development of type 2 DM at
bay. Overtime, beta-cell
dysfunction develops,
(McCance et al., 2019).
In secondary (central)
hypothyroidism, the pituitary gland vasoconstriction, which is mediated
fails to synthesize an adequate
amount of TSH. Common causes of Tubuloglomerular feedback
this disorder include pituitary
tumors that constrict surrounding
pituitary cells, or results
secondarily from treatment of these decreases – the GFR declines
tumors (McCance et al., 2019).
through autoregulatory mechanisms
consisting of inward arteriolar
dilation and outward arteriolar
by angiotension 2.
mechanisms help to maintain GFR
as well as the distal tubular nephron
flow. As the filtration pressure
(McCance et al., 2019).
In Intrarenal AKI, injury results
from either ischemic acute tubular
necrosis (ATN), acute
glomerulonephritis, nephrotoxic
ATN, vascular disease, or
interstitial disease (McCance et al.,
2019). ATN can be either
postischemic or nephrotoxic. In
postischemic ATN, a combination
of hypotension, hypoxemia and
hypoperfusion decrease levels of
adenosine triphosphate (ATP),
which generates oxygen free
radicals causing cell injury,
swelling and death (McCance et al.,
2019). Tubular injury is caused by
the activation of neutrophils,
macrophages and lymphocytes, as
well as the release of inflammatory
causing a decrease in insulin
activity, due to a reduction in
both beta-cell mass and
function (McCance et al.,
2019). Alpha cells of the
pancreas become less
receptive to glucose
hindrance, causing increased
glucagon secretion (McCance
et al., 2019). This causes
elevated blood glucose levels
in the individual. Amylin is
also a beta-cell hormone that
is found to be decreased in
type 2 DM. In normal
functioning, amylin
suppresses glucagon released
by alpha cells, delays gastric
emptying and acts as a satiety
agent (McCance et al., 2019).
Additionally, incretins are a
group of metabolic hormones
that are released after eating,
which activate the secretion
of insulin from beta-cells. In
type 2 DM, responsiveness to
these hormones are decreased
(McCance et al., 2019).
cytokines (McCance et al., 2019).
Damage occurs to the proximal
tubular epithelium, as well as
sloughing of the brush border,
causing a disruption in the
transportation of molecules, and the
formation of tubular granular casts
seen on urinalysis (McCance et al.,
2019). Location of injury can be
found along nephron tubules, the
outer medulla, cortex and scattered
along the tubular epithelium
(McCance et al., 2019).
Nephrotoxic ATN has been found
to be caused by certain drugs that
accumulate in the renal cortex.
Drugs / substances found to cause
renal failure include:
 Radiocontrast
 Antibiotics
(aminoglycosides)
 Heavy metals
 Bacterial toxins
 Carbon tetrachloride
 Methoxyflurane
Injury by nephrotoxins usually
occurs in the proximal tubules
(McCance et al., 2019)
 In Postrenal AKI, kidneys are
affected bilaterally by obstruction
of the urinary tract. This
obstruction causes increased
intraluminal pressure occurring
above the site, causing a continuous
decrease in GFR (McCance et al.,
2019). Often caused after
catheterization of the ureters, in
which the resulting edema obstructs
the tubular lumen (McCance et al.,
2019).
Plan of Care There is not an established
pharmacotherapy for AKI (Koza,
2016). Measures taken in
prevention of AKI are stressed.
Individual therapy and monitoring
are indicated until renal function
has resumed to baseline (McCance
et al., 2019). Management includes:
 Monitoring blood pressure
 Correcting fluid /
electrolyte imbalances
 Maintaining diet / nutrition
 Preventing infections
 Monitoring fluid output
(in’s and out’s)
 Considering
contraindications of certain
drugs due to the risk of
 toxicity (radiocontrasts,
aminoglycosides)
***AVOID: Fluid overload***

In severe cases of hyperkalemia,

acidosis or fluid overload, patients
with AKI might necessitate renal
replacement therapy (RRT), in
which continuous, intermittent or
peritoneal dialysis is initiated
(Koza, 2016).

Other treatment for hyperkalemia

may include diet restrictions, non-
potassium-sparing diuretics, and /
or cation ion exchange resins.
Administration of glucose and
insulin, or an infusion of sodium
bicarbonate or albuterol forces
potassium back into the cells
(McCance et al., 2019)

Educate patient: Review that it may

take 3-12 months before renal
function resumes to a normal state.
Also include that AKI predisposes
them to the development of other
disorders, such as kidney failure,
cardiovascular events, and stroke
(McCance et al., 2019).
Analysis
For this case study, missing factors
included:
 Patient’s height
 Occupation
 Medications and/or
compliance with
medications
 Exposure to harmful
substances
 Lifestyle (smoking, alcohol,
sleep)
 Diet / exercise
 Onset of symptoms
 Family history

It is my determination / working
diagnosis that this patient is
suffering from AKI. I ruled out type
2 DM as the main diagnosis, even
with an A1c of 6.9, history of HTN,
and complaints fatigue and pruritis.
The patient is not obese, which is a
main factor in the development of
type 2 DM. Unsure of diet, exercise
routine or family history - although
type 2 DM did not explain the
patient’s abnormal lab values, or
the complaint of nausea and
vomiting.
I ruled out hypothyroidism as the
diagnosis for this patient due to the
patient’s TSH being within normal
limits. The patient is also male –
hypothyroidism is most often seen
in women and the elderly. The
patient does not have a history of an
autoimmune disorder, and as far as
we know – no family history. While
the patient does present with
moderate anemia, as well as c/o
edema to bilateral lower extremities
and fatigue, hypothyroidism does
not explain his complaints of
itching, N/V or other abnormal lab
values.

AKI is the best answer for this case

study due to the overwhelming
similarity among signs, symptoms
and lab values – consistent with
AKI. According to the case study,
the patient has a “long standing”
history of HTN, which is a
comorbidity that places him at
higher risk. His complaints of
fatigue, pruritis, and N/V are all
symptoms involved in AKI. Lower
extremity edema is seen due to
fluid volume overload associated
with fluid retention, caused by
 venous congestion and a decreased
GFR. Abnormal lab values
consistent with AKI include:
 Anemia
 Hyperkalemia
 Increased BUN and
creatinine
 Hyperphosphatemia
 Urinalysis remarkable for
casts and protein
Unsure of exact etiology, the
patient may be suffering from AKI
due to a combination of all risk
factors. Potentially nephrotoxic
ATN, more information about
medications and substance
exposure is needed to confirm.
References See below See below See below

Chaker, L., Bianco, A. C., Jonklaas, J., & Peeters, R. P. (2017). Hypothyroidism. Lancet (London, England), 390(10101),
1550–1562. https://doi.org/10.1016/S0140-6736(17)30703-1

Kolb, H., & Martin, S. (2017). Environmental/lifestyle factors in the pathogenesis and prevention of type 2 diabetes. BMC
medicine, 15(1), 131. https://doi.org/10.1186/s12916-017-0901-x

Koza Y. (2016). Acute kidney injury: current concepts and new insights. Journal of injury & violence research, 8(1), 58–62.
https://doi.org/10.5249/jivr.v8i1.610

McCance, K. L., & Huether, S. E. (2019). Pathophysiology: The biologic basis for disease in adults and children.
 Nie, S., Tang, L., Zhang, W., Feng, Z., & Chen, X. (2017). Are There Modifiable Risk Factors to Improve AKI?. BioMed
research international, 2017, 5605634. https://doi.org/10.1155/2017/5605634