Topics Covered: Basic kidney physiology (just enumeration). Manifestations of renal impairment. AKI vs. CRF , definitions, causes and their classifications (in brief) . Clinical evaluation of a case of renal failure. indications for renal replacement therapy. Approach for real-Life patient with renal impairment: group-case discussion.

1. (for undergraduates 3rd year Integrated Medicine)
Compiled by Ahmed Redwan, 2021 © COPYRIGHTED
Assist. Lecturer Int. Med. Depart.
El-Minia University, EGYPT.

2. Topics Covered:
 Basic kidney physiology (just enumeration).
 Manifestations of renal impairment.
 AKI vs. CRF , definitions, causes and their
classifications (in brief) .
 Clinical evaluation of a case of renal failure.
 indications for renal replacement therapy.
 Approach for real-Life patient with renal
impairment: group-case discussion.

3. 1. Plasma ultrafiltration; excretion of water soluble toxins and
maintain the volume balance (euvolemia).
2. Maintain electrolytes balance.
3. Maintain acid-base balance.
4. Endocrinal; erythropoietin (EPO) production guarding
against anemia, and final Vitamin D activation.
5. Renin Angiotensin Aldosterone System (RAAS); control of
BP.
6. Metabolic; gluconeogenesis (extra hepatic site for
Glucose production), storage and metabolism for folic acid
& vitamin B12.
7. Immune; contribute of both humoral and cellular immunity.

7. CLINICAL EVALUATION OF a case of renal failure:
The history, and physical examination aimed at :
 Differentiate between AKI & CKD & acute on top of chronic.
 Establishing possible cause (s) & D.D & Provisional D.
 Finding evidence of associated multisystem disease.
 Explore the possibility for correctable cause (s) e.g. remove
the stone in obstructive uropathy or UTI treatment.
 Evaluation & grading renal function .
 Estimate complication (s) , its life-threatening emergency, and
need for RRR.
 Report previous management to which the patient was
subjected to and its outcome e.g. urothroscopy , renal biopsy.
 Choose individualized plan of management based on patient
& disease stage characteristics.

20. 1- Skin; Pruritus. Pigment alteration (pallor due anemia.
Yellowish color, due to retained urochromes and carotene.
Brownish hyperpigmentation is common mostly in a sun-
exposed distribution, these gives the earthy colour face).
Dryness of the skin. Half-and-half nails (The distal part of
fingernails become brownish in color). Uremic frost (increase
evaporation of urea through sweat glands results in the
deposition of urea crystals on the skin). Alopecia.
2- Gastrointestinal; are among the earliest and most common
signs of the uremia. Metallic taste, loss of appetite, anorexia,
nausea, vomiting, and weight loss. Severe uremia may also
experience stomatitis, enteritis or GI bleeding.

21. 3- Cardiovascular; Hypertension, left ventricular
hypertrophy and congestive heart failure. Accelerated
atherosclerosis and IHD. Metastatic calcification in the
myocardium, cardiac valves, and arteries. Arrhythmias, and
sudden cardiac death. Pericarditis, pericardial tamponade
or constrictive pericarditis.
4- Pulmonary; pulmonary edema. Pneumonitis. Pleuritis.
Pleural effusion.

22. 5- Neurologic; Central nervous system (CNS);
Impaired cognitive function and memory.
Disturbances of sleep. Encephalopathy;
Lethargy, irritability, asterixis, seizures, and
later on coma.
Peripheral nervous system; progressive
symmetrical sensory neuropathy in a glove-
and-stocking distribution. Decreased distal
tendon reflexes and loss of vibratory
perception. Restless legs, foot drop, or wrist
drop.

23. 6- Muscle; Generalised myopathy may occur due
to a combination of poor nutrition,
hyperparathyroidism, vitamin D deficiency and
disorders of electrolyte metabolism. Gout and
pseudogout.
7- Endocrine/metabolic; Hyperparathyroidism.
Increased insulin resistance. Amenorrhea.
Impotence. Hyperlipidemia.
8- Acid- base/electrolyte; Metabolic acidosis
(Kussmaul’s breathing). Hyperkalemia. Fluid
overload. Hypocalcemia. Hyperphosphatemia.
Hypermagnesemia.

24. 9- Immune dysfunction; Cellular and
humoral immunity is impaired in advanced
CKD. Which is the second most common
cause of death in dialysis patients, after
cardiovascular disease.

25. 10- Haematological; There is an increased bleeding
tendency in advanced CKD, which manifests as
cutaneous ecchymoses and mucosal bleeds, due to
platelet dysfunction or coagulopathy. Causes of
anaemia in chronic kidney disease are:
• Deficiency of erythropoietin
• Toxic effects of uraemia on marrow precursor cells
• Reduced red cell survival
• Increased blood loss due to capillary fragility and
poor platelet function
• Reduced intake, absorption and utilisation of dietary
iron.

26. 11- Metabolic bone disease; Disturbances of calcium and
phosphate metabolism are almost universal in advanced
CKD, and various types of metabolic bone disease may
also occur, including osteitis fibrosa cystica, osteomalacia
and osteoporosis.
There is impaired conversion of 25-hydroxyvitamin D
to its active metabolite, 1,25-dihydroxyvitamin D, thereby
causing hypocalcaemia, and increased PTH production by
the parathyroid glands and hyperphosphataemia develops.
In some cases, tertiary hyperparathyroidism
supervenes, due to autonomous production of PTH by the
enlarged parathyroid glands; this presents with
hypercalcaemia.

27. Indications for dialysis in patients with CKD include:
• Severe metabolic acidosis (refractory to medical
management).
• refractory hyperkalemia.
• uremic pericarditis.
• uremic encephalopathy such as confusion, asterixis, or
seizures.
• Fluid overload or pulmonary edema refractory to diuretics.
• Intractable gastrointestinal symptoms e.g. refractory
vomiting.
• Malnutrition with failed medical management.
• Bleeding diathesis attributable to uremia
• The GFR is 15 mL per minute or less and there are no
apparent reversible causes of kidney failure.

31. Acute Renal Failure
Clinical Assessment (Volume Status,
Urinalysis and Ultrasound)
Pre-Renal Intra-Renal Post-Renal
Absolute Decrease
In ECF Volume
GI losses
Hemorrhage
Decreased
Renal
Blood Flow
Heart failure
Renal artery
stenosis
Altered Intra-Renal
Hemodynsmics
Drug-induced
NSAIDS/COX-2
Inhibitors
Calcineurin inhibitors
ACE inhibitors
AII Receptor Blockers
Sepsis
Hypercalcemia
Cirrhosis/Hepatorenal
syndrome
Abdominal compartment
syndrome
Tubulointerstitial
Disorders
Tubular Injury
Ischemic
Nephrotoxic
Interstitial Nephritis
Allergic-type
NSAID-type
Glomerular Disorders
Glomerulonephritis
Thrombotic
microangiopathies
Atheroembolic
disease
Anatomic Obstruction
Bladder Outlet
Prostate
Pelvic Tumor
Ureteral
Tumor
Stones
Stricture
Tubular Obstruction
Crystals
Calcium oxalate
(Ethylene glycol
poisoning)
Drugs
Indinovir
Methotrexate
Proteins
Myeloma cast
nephropathy
ATN

32. 1.Major extrarenal artery or venous occlusion
2. Disorders of the small intrarenal vasculature
can result in AKI (e.g., vasculitis, thrombotic
microangiopathy, malignant hypertension,
eclampsia, postpartum states, disseminated
intravascular coagulation, scleroderma).
3. All forms of acute glomerulonephritis
4. Acute inflammation and space-occupying
processes of the renal interstitium (e.g., drug-
induced, infectious, and autoimmune disorders;
leukemia; lymphoma; sarcoidosis).

33. 5. There are also significant geographic differences
in the causes of AKI. Obstetric AKI remains more
common in emerging countries.
6. There are also different patterns of accidental and
deliberate self-poisoning. In Africa, herbal toxins are
a common cause of AKI.
7. Contrast-induced Nephropathy.
8. Severe hemolysis may also occur in a. Malaria b.
Drugs in association with glucose-6-phosphate
dehydrogenase deficiency c. After spider, snake, and
insect bites In the hospital setting, prerenal uremia
and acute tubular necrosis (ATN) account for the
majority of AKI cases.

35. Causes & Risk factors of
AKI
Exposures
•Sepsis
•Critical illness
•Circulatory shock
•Burns
•Trauma
•Cardiac surgery
(especially with CPB)
•Major noncardiac surgery
•Nephrotoxic drugs
•Radiocontrast agents
•Poisonous plants and
animals
Susceptibilities
Dehydration or volume
depletion
Advanced age
Female gender
Black race
CKD
Chronic diseases (heart,
lung, liver)
Diabetes mellitus
Cancer
Anemia

36. Natural History of AKI

38. • The causes of CKD are generally
untreated systemic and renal/urological
diseases.
the most common being diabetic
nephropathy, hypertensive nephropathy,
APKD, chronic GN, chronic
pyelonephritis/reflux, chronic obstruction and
renovascular disease.
• The frequency of CKD increases with age.

40. The great majority of CKD patients with slowly
progressive disease are asymptomatic until GFR falls below
30 mL/min/1.73 m2 (stage 4 or 5).
Nocturia, due to the loss of concentrating ability and
increased osmotic load per nephron, can be an early
symptom. Oliguria occur in the late stages of CKD.
In ESRD (stage 5) there may be pruritus, anorexia,
nausea and vomiting. Later, hiccups, unusually deep
respiration related to metabolic acidosis (Kussmaul's
respiration), muscular twitching, fits, drowsiness and coma
ensue.
These clinical features reflect a loss of the main roles of
the kidney and always multisystemic.
Some patients present with only one of each of the
features, but most will have a combination.

43. 
Dark urine which is dipstick
positive for blood but
contains no red cells or
casts on microscopy is likely
to be due to myoglobinuria
Hematuria

46. Patients are considered to have SLE if they meet 4 of the
following 11 criteria:
 Malar rash
 Discoid rash
 Photosensitive rash
 Oral ulcers
 Nonerosive arthritis in 2 or more joints
 Pleuritis or pericarditis
 Glomerulonephritis or proteinuria
 Seizures or psychosis
 Hemolytic anemia, leukopenia, lymphopenia, or
thrombocytopenia
 Immunologic laboratory abnormalities, such as antibodies to
double-stranded DNA or the SM antigen or a false-positive
serologic test for syphilis
 Positive ANA test that is not caused by a medication

51. Haemolytic uraemic
syndrome is
characterised by a
triad of:
microangiopathic
haemolytic anaemia
(MAHA),
thrombocytopaenia
and renal failure.

55.  The majority of renal diseases do not lead to
symptoms that patients will report.
 Many cases of renal dysfunction discovered accidently
during routine medical examinations.
 The symptoms are widely variable between patients at
time of presentation and often multisystem.
 Even the same patient can be presented by different
manifestations allover the disease course.
 The disease nature may be slowly progressive taking
months (CKD) or deteriorates very aggressively
leading to failure within days (AKI).
 However, specific questioning may reveal edema,
hypertension, foamy urine, or urinary abnormalities
during prior routine testing (e.g., during routine medical
examinations) helping in the determination of disease
onset and differentiating AKI from CKD.

56. Name
Age (common):
DM type 1 (young)
Infection , SCLD, Rhod A and SLE (13-35)
HTN and DM type 1 (middle age)
Malignancy (old age).

57. Male
IgA Nephropathy (2:1)
Post Strept.GN
Goodpasture syndrome.
Female
9:1)
)
Lupus N
vasculitis

58.  occupations certain jobs are associated with
an increased risk of developing diseases
which can present with renal problems. For
example, livestock and arable farming is
associated with an increased risk of
developing anti - neutrophil cytoplasmic
antibody (ANCA) - associated vasculitis.
 Tubulo-interstitial nephritis are more common
after chemical/radiological exposure.

59. Marietal status
Lupus nephritis activity are commonly
progressive with each pregnency since
its first presentation.
Preclampsia and its related nephropathy
may lead to critical outcomes for mother
and baby.

60. Smoking history:
smoking is a risk factor for renovascular
disease and is associated with pulmonary
haemorrhage in patients with Goodpasture ’ s
disease).
Also considered independent risk factor
for CRF.
Intravenous drug use (IVDU) is a risk factor for
hepatitis B/C/HIV, which are associated with a
variety of GN.

61. 1.Urine abnormalities
• Amount: A reduced amount of urine ( < 400
mL/day) is termed oliguira. An absence of
urine production is termed anuria ( < 100
mL/day) .
Oliguria occurs in nephritic syndrome, acute
renal failure (ARF) and chronic end - stage
renal failure (ESRF). Absolute anuria
suggests a complete obstruction to the
outflow of urine (e.g. prostatic disease), a
vascular catastrophe or acute cortical
necrosis.

62. An increased production of urine is termed polyuria
(urine output > 3 L/24 h). This may occur as a
result of:
 Insensitivity to ADH (nephrogenic diabetes
insipidus)
 Osmotic diuresis (hyperglycaemia, hypercalciuria)
 Chronic kidney disease (CKD) (inability of the
diseased tubular cells to appropriately move Na
and hence concentrate urine)
Nocturia (frequent urination at night) in uncontrolled
DM, APKD, prostatitis, some cases of TIN.

63. Colour :
normally, urine should be clear to light yellow in
colour (depending on concentration). ‘ Coke - coloured ’
is seen in nephritic syndrome, where there is glomerular
haematuria. ‘ Tea - coloured ’ urine is seen in
myoglobinuria (usually secondary to rhabdomyolysis).
Macroscopic haematuria (where urine is obviously blood
- stained) may be due to bleeding in the upper (e.g. IgA
nephropathy) or lower urinary tract (e.g. bladder cancer,
renal calculi).
Frothy urine is observed if there is heavy
proteinuria. Other causes of discoloured urine include
rifampicin or beetroot ingestion (pink - red) and
cholestatic jaundice (bright/ strongly coloured yellow).
Discolouration of urine on standing may occur in
alkaptonuria or porphyria.

64. Dysuria (pain whilst passing urine): this
classically occurs in UTI or in urethritis (if
untreated leading to chronic GN).
2. Loin pain: this can occur due to renal calculi
(stones), infection, IgA nephropathy, loin pain
haematuria, and polycystic kidney disease.
Renal colic (due to the passage of a renal
calculus through the ureter) is usually
agonizingly painful.

65. 3. Oedema: occurs if there is volume overload (increased
hydrostatic pressure) or in nephrotic syndrome where heavy
proteinuria leads to reduced oncotic pressure.
4. Symptoms of hypertension, e.g. headache, blurred vision or
fits (if severe). (can be a cause of, or occur as a result of renal
impairment)
5. Symptoms of anaemia (secondary to erythropoietin (EPO)
deficiency), e.g. tiredness, dyspnoea.
6. Symptoms of uraemia such as nausea/vomiting, chest pain
associated with pericarditis or confusion due to uraemic
encephalopathy.
7. Symptoms of hyperphosphataemia such as itchiness, lethargy
8. Multisystem diseases associated with glomerular disease
include diabetes, hypertension, amyloid, lupus, and vasculitis.

66. Has the patient started on any new drugs? Such a
history may suggest acute tubulointerstitial nephritis
(TIN), particularly if associated with a rash. Some drugs
are associated with the development of SLE (e.g.
hydralazine). • Is the patient taking any nephrotoxic
medications? (ACEI), (NSAID), gentamicin, lithium,
amphotericin, cisplatin (directly toxic to tubules);
Certain drugs and toxins may cause glomerular
disease; these include
a. Minimal change disease (MCD; nonsteroidal anti-
inflammatory agents [NSAIDs] and interferon),
b. Membranous nephropathy (penicillamine; NSAIDs;
mercury, for example, in skinlightening creams),
c. FSGS (pamidronate, heroin), and HUS (cyclosporine,
tacrolimus, mitomycin C, oral contraceptives).

67. Other drugs; ciclosporin - A (alter renal blood
flow and can lead to HTN especially if
unmonitored); NSAID, antibiotics, proton
pump inhibitors (PPI) (associated with
interstitial nephritis); gold, penicillamine (can
cause proteinuria).
Is the patient taking any drugs which are
predominantly excreted by the kidneys, e.g.
digoxin or allopurinol? In such cases, the
dose of the drug should be reduced if there is
a signifi cant renal impairment.

68. Has the patient ever had any renal problems previously?
Have they ever had their kidney function assessed? This is
useful if trying to delineate between acute and chronic GN.
Is there a PMH of diseases which can cause chronic
kidney disease? • Diabetes mellitus (diabetic nephropathy) •
Hypertension (can be a cause of, or occur as a result of renal
impairment) • Vascular disease, including peripheral vascular
disease, myocardial infarction, cerebrovascular disease. A past
history of such diseases marks out the patient as an arteriopath
who may also have renovascular disease • Prostatic
hypertrophy (obstructive uropathy) • Recurrent UTI (chronic
pyelonephritis) • Recurrent renal calculi (nephrocalcinosis)

69. Is there a PMH of diseases or other illness prior to
presentation which can cause GN? e.g. pharyngitis
(which may be associated with IgA nephropathy
(synpharyngitic GN) or post - streptococcal
glomerulonephritis (GN)), infective endocarditis, and
certain viral infections) may also be associated with a
variety of glomerular diseases.
Vomiting/ diarrhea/blood loss (all of which
predispose to volume depletion and pre - renal failure),
sepsis (risk factor for pre - renal failure/ATN) or back
pain (which can be associated with myeloma).

70. Many autoimmune diseases are systemic
and affect multiple organ systems. Thus, there
may be non – specific symptoms such as fever,
night sweats, lethargy and malaise.
A failure to enquire about or recognise the
importance of such relatively non - specifi c
systemic symptoms can lead to a delay in
diagnosis of some serious autoimmune
diseases, particularly systemic vasculitis.
FMF also presented by fever, and other non
specific symptoms.

71. In addition to systemic symptoms, there may also be
evidence of inflammation in other systems such as joints
(arthralgia), eyes (red eyes due to anterior uveitis, dry eyes
due to keratoconjunctivitis sicca), gastrointestinal tract
(mouth ulcers, abdominal pain), genitourinary ulcers, skin
(photosensitivity rash, discoid lupus, purpuric rash of
vasculitis) or symptoms typical of a systemic vasculitis (e.g.
sinusitis, ear ache, hearing loss, shortness of breath,
haemoptysis).
The occurrence of pulmonary haemorrhage in
association with acute renal failure secondary to a rapidly
progressive glomerulonephritis is known as pulmonary -
renal syndrome, and is important to recognize.

72. Malignant neoplasms are associated with
glomerular disease. Patients will occasionally
present with the renal disease as the first
manifestation of a tumor. These include:
a. Lung, breast, and gastrointestinal carcinoma
(membranous nephropathy)
b. Hodgkin’s disease (MCD)
c. Non-Hodgkin’s lymphoma
(membranoproliferative glomerulonephritis
[MPGN])
d. Renal carcinoma (amyloid).

73. A positive family history may also be obtained
in some cases.
The most common genetic disorder affecting
the kidneys is adult (autosomal dominant)
polycystic kidney disease (APKD). New mutations
occur in only 5% of cases, although many patients
will not be aware of a positive family history of
disease. Closer questioning or discussion with
older relatives may prompt recall of a family
member who died of ‘ kidney trouble ’ or ‘ brain
haemorrage.

74. Other causes of familial renal disease may
include
a. Alport’s syndrome (especially if it is associated
with hearing loss)
b. Uncommon familial forms of IgA nephropathy
c. Focal segmental glomerulosclerosis (FSGS)
d. Hemolytic-uremic syndrome (HUS), and other
rare conditions.

75. 1. Is the patient sick or HEMODYNAMICALLY stable? It is
important to identify this early as some patients with
acute renal failure (AKI) that may REQUIRES (ICU) care.
Temperature : a fever may indicate infection or systemic
autoimmune disease.
Pulse: abnormalities associated with complications of
electrolytes imbalance (K+), fever, hypervolemia.
R.R. Kussmaul’s breathing in metabolic acidosis,
pulmonary edema, associated chest infection.
B.P. cause & result may be severely elevated (HTN
emergency) if low or postural
drop then it is likely that there is hypovolemia.

76. The presence of dependent pitting edema suggests the
nephrotic syndrome that should be differentiated from
heart failure, or cirrhosis.
a. In the nephrotic subject, edema is often periorbital in
the morning.
b. As it progresses, edema of genitals and abdominal
wall becomes apparent, and accumulation of fluid in
body spaces leads to ascites and pleural effusions. c.
Edema is unpleasant; it leads to feelings of tightness in
the limbs and a bloated abdomen. There are practical
problems of clothes and shoes no longer fitting. d. The
edema becomes firm and stops pitting only when it is
long-standing. E.sacral oedema in bed - bound patients.

77. 3. Chronic hypoalbuminemia is also associated with loss
of normal pink color under the nails, resulting in white
nails (Leuconychia) or white bands if the nephrotic
syndrome is transient (Muehrcke’s bands).
4. Xanthelasmas may also be present as a result of the
hyperlipidemia associated with the nephrotic
syndrome.
5. The presence of pulmonary signs should suggest one
of the pulmonary-renal syndromes.
6. Palpable purpura may be seen in vasculitis, systemic
lupus, cryoglobulinemia, or endocarditis
7. Nailfold infarcts, necrotic areas (signs of
vasculitis/endocarditis)

78. Skin rashes : purpuric lesions (associated with
vasculitis), photosensitivity rash (usually on sun -
exposed areas such as dorsum of forearms, neck
and face – seen in SLE), maculopapular
erythematous rash (drug associated), petechial
rash (associated with thrombocytopaenia, e.g. as
seen in haemolytic uraemic syndrome).
Mouth : in a renal transplant patient, there may
be gingival hypertrophy if the patient is on long -
term ciclosporin. SLE and Behçet ’ s disease are
associated with mouth ulceration. Amyloidosis is
associated with macroglossia.

79. Eyes : conjunctivitis and anterior uveitis
both present with red eyes and can occur in
autoimmune conditions which are also
associated with renal involvement (e.g.
rheumatoid arthritis can cause a
keratoconjunctivitis and may be associated
with amyloidosis).
In addition, fundoscopy should be
performed in order to assess whether there is
retinopathy associated with hypertension or
diabetes mellitus.

80. Small joints of the hands for signs of
arthritis (heat, swelling, pain, erythema, the
classic signs of inflammation) which can
occur in some systemic autoimmune
diseases that affect the kidney, e.g. SLE,
rheumatoid arthritis.

81. Assess intravascular volume status, as
volume depletion is a cause of ARF and fl uid
overload can occur as a consequence of
oligo/anuria.
Elevated JVP suggests volume overload,
low JVP suggests volume depletion
Blood pressure (BP) (if low or postural
drop then it is likely that there is
hypovolaemia).

82. Heart sounds : murmurs may be audible
in endocarditis (which can be associated with
GN due to deposition of circulating immune
complexes in the glomeruli).
Mitral regurgitation or mitral valve
prolapse is associated with APKD.
An aseptic endocarditis can occur in SLE
(Libmann Sachs endocarditis).
Severe uraemia can lead to pericarditis
and a pericardial rub.

83. Pleural effusion (ipsilateral reduced expansion,
reduced breath sounds, stony dull percussion note)
can occur in nephrotic syndrome.
Pulmonary oedema (increased respiratory rate,
reduced oxygen saturations, bibasal crepitations) can
occur if there is volume overload.
Coarse inspiratory crepitations may also occur if
there is pulmonary haemorrhage (seen in Goodpasture
’ s disease and ANCA - associated vasculitis).
Pulmonary fibrosis (reduced oxygen saturations,
reduced expansion, fine end - inspiratory crepitations)
can be associated with ANCA - associated vasculitis.

84. Hepatosplenomegaly may occur secondary to
cirrhosis with portal hypertension secondary to
hepatitis B/C (both associated with GN) or
secondary to amyloidosis (can affect the kidney,
causing nephrotic syndrome and renal
impairment).
Palpable kidneys : occurs in APKD or renal
tumour, or occasionally in amyloidosis.
(hydronephrosis)
Splenomegaly may be observed in SLE. •
Palpable kidneys : occurs in APKD or renal
tumour, or occasionally in amyloidosis.

85. Abdominal aortic aneurysm (associated
with renovascular disease and retroperitoneal
fi brosis).
Renal bruits +/ − femoral bruits:
associated with renovascular disease.
Renal transplant in situ (usually a
palpable mass in the left or right iliac fossa,
with overlying ‘ hockey - stick ’ scar) (Figure).
There may also be a scar visible from
previous peritoneal dialysis catheter insertion.

87. Uraemia can be associated with encephalopathy
(i.e. impairment of conciousness +/ − confusion).
, also aggressive initiation of hemodialysis may lead to
cerebral edema (disequilibrium syndrome).
Deafness (usually conductive) may occur in ANCA
- associated vasculitis (particularly Wegener ’ s
granulomatosis). Sensorineural deafness is a feature
of Alport ’ s syndrome and some rare tubular diorders
(where the same pumps are found in the ear as in
tubular cells). • Patients with long - standing diabetes
with associated microvascular disease may have signs
of neuropathy (peripheral or autonomic) as well as
nephropathy.

88. Vasculitides (particularly Churg - Strauss
syndrome) are associated with peripheral
neuropathy or mononeuritis multiplex.
Some patients with SLE have
neuropsychiatric features, including poor
memory, psychosis and depression.
Systemic amyloidosis is associated with
peripheral neuropathy (peripheral nerves may
enlarge and become palpable) and/or
autonomic neuropathy (evidenced by loss of
heart rate variability and an increase in
postural drop).

89.  A 55-year-old woman is referred to your office because of a
serum creatinine of 2.5 mg/dL noted on routine labs 3 weeks prior.
 She denies dysuria, gross hematuria, or change in urine output.
 She urinates at least two times per night. She is obese and has
chronic back pain. She is not taking any prescription medications.
 Blood pressure is 135/78 mmHg. Pulse is 82 beats per minute.
 She has trace to 1+ edema to her mid-shin. Remainder
of her physical exam is unremarkable.
 Repeat serum creatinine is 2.6 mg/dL.
 Urine sediment is a bland.
 What is your approach to diagnosis and management
of this patient?
-89-
Case

90. Case Revised
-90-
 The case illustrates just how important meticulous history taking is.
Further history was obtained which revealed that she had been taking
800 mg of ibuprofen three times daily for the past several years due to
her chronic back pain. She reported taking no other over-the-counter or
herbal substances.
 There were no constitutional symptoms or family history of renal
diseases. Her exam was unremarkable. Previous laboratory data was
not available.
 The urine sediment was bland. Protein excretion was 1 g via spot
ratio. Renal ultrasound showed small (9 cm) bilateral kidneys with
increase in cortical echogenicity. No masses, cysts, or hydronephrosis
were noted.
 A presumptive diagnosis of chronic tubulointerstitial disease was
made and the patient was advised to discontinue her ibuprofen.
 Her creatinine and proteinuria were routinely monitored and treatment
focused on slowing CKD progression and management.