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(for undergraduates 3rd year Integrated Medicine)
Compiled by Ahmed Redwan, 2021 © COPYRIGHTED
Assist. Lecturer Int. Med. Depart.
El-Minia University, EGYPT.
CLINICAL EVALUATION OF GLOMERULAR
DISEASE
The history, and physical examination
aimed at :
 Clinical differentiation of major nephrological syndromes.
 Establishing possible cause(s).
 Finding evidence of associated multisystem disease
 Excluding confounding non-glomerular disease (e.g.
urological)
 Evaluation & grading renal function.
 Estimate complication (s)
 Report previous management to which the patient was
subjected to and its outcome.
Renal disease generally presents in three ways:
• hypertension
• urine abnormalities (proteinuria/
haematuria) & its clinical presentations.
• manifestations of abnormal renal function
tests/ (GFR).
These clinical features reflect a loss of the main
roles of the kidney.
Some patients present with only one of each of the
features, but most will have a combination.
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
Haemolytic uraemic
syndrome is
characterised by a triad of
;
microangiopathic
haemolytic anaemia
(MAHA),
thrombocytopaenia and
renal failure.
The majority of glomerular 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
or deteriorates very aggressively leading to failure within days
However, specific questioning may reveal edema,
hypertension, foamy urine, or urinary abnormalities during prior
routine testing (e.g., during routine medical examinations).
Name
Age (common): MCD infancy, Post infectious
GN (5-12 y), Lupus Nephritis (14-35 y)
Ch.GN & Memb.GN (30-50y) & 2ry FSGN
with advanced age
Male
IgA Nephropathy (2:1)
Post Strept.GN
Good-pasture syndrome (1.5 : 1)
Female
9:1)
)
Lupus N
vasculitis
 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.
Marietal status
Lupus nephritis activity are commonly progressive
with each pregnancy since its first presentation,
even termination of pregnancy is indicated in
rapidly deterioration of renal function.
Secondary antiphospholipid syndrome – commonly
associated with lupus – is claimed for recurrent
abortion.
Preclampsia and its related nephropathy may lead
to critical outcomes for mother and baby.
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.
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.
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 & prostatitis, sometimeTIN.
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.
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.
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.
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).
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 significant renal impairment.
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 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).
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).
A positive family history may also be
obtained in some cases. 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.
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+).
R.R. Kussmaul’s breathing in metabolic
acidosis, tachypnea in renal failure.
B.P. cause & result may be severely elevated
(HTN emergency)
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.
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)
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.
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.
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.
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).
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.
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.
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).
Splenomegaly may be observed in SLE. •
Palpable kidneys : occurs in APKD or renal tumour, or
occasionally in amyloidosis.
Abdominal aortic aneurysm (associated with
renovascular disease and retroperitoneal fibrosis).
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.
GN complications e.g. Uraemia can be
associated with encephalopathy (i.e. impairment of
conciousness +/ − confusion).
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.
Vasculitides (particularly Churg - Strauss
syndrome) are associated with peripheral
neuropathy or mononeuritis multiplex. Some
patients with SLE have neuropsychiatric
features, including poor memory 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).
‫هللا‬ ‫بحمد‬ ‫تم‬

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Glomerulonephritis: History taking and examination.

  • 1. (for undergraduates 3rd year Integrated Medicine) Compiled by Ahmed Redwan, 2021 © COPYRIGHTED Assist. Lecturer Int. Med. Depart. El-Minia University, EGYPT.
  • 2. CLINICAL EVALUATION OF GLOMERULAR DISEASE The history, and physical examination aimed at :  Clinical differentiation of major nephrological syndromes.  Establishing possible cause(s).  Finding evidence of associated multisystem disease  Excluding confounding non-glomerular disease (e.g. urological)  Evaluation & grading renal function.  Estimate complication (s)  Report previous management to which the patient was subjected to and its outcome.
  • 3.
  • 4. Renal disease generally presents in three ways: • hypertension • urine abnormalities (proteinuria/ haematuria) & its clinical presentations. • manifestations of abnormal renal function tests/ (GFR). These clinical features reflect a loss of the main roles of the kidney. Some patients present with only one of each of the features, but most will have a combination.
  • 5.
  • 6. 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
  • 7.
  • 8.
  • 9. Haemolytic uraemic syndrome is characterised by a triad of ; microangiopathic haemolytic anaemia (MAHA), thrombocytopaenia and renal failure.
  • 10.
  • 11.
  • 12.
  • 13.
  • 14. The majority of glomerular 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 or deteriorates very aggressively leading to failure within days However, specific questioning may reveal edema, hypertension, foamy urine, or urinary abnormalities during prior routine testing (e.g., during routine medical examinations).
  • 15. Name Age (common): MCD infancy, Post infectious GN (5-12 y), Lupus Nephritis (14-35 y) Ch.GN & Memb.GN (30-50y) & 2ry FSGN with advanced age
  • 16. Male IgA Nephropathy (2:1) Post Strept.GN Good-pasture syndrome (1.5 : 1) Female 9:1) ) Lupus N vasculitis
  • 17.  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.
  • 18. Marietal status Lupus nephritis activity are commonly progressive with each pregnancy since its first presentation, even termination of pregnancy is indicated in rapidly deterioration of renal function. Secondary antiphospholipid syndrome – commonly associated with lupus – is claimed for recurrent abortion. Preclampsia and its related nephropathy may lead to critical outcomes for mother and baby.
  • 19. 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.
  • 20. 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.
  • 21. 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 & prostatitis, sometimeTIN.
  • 22. 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).
  • 23. 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.
  • 24. 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.
  • 25. 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.
  • 26. 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).
  • 27. 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).
  • 28. 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 significant renal impairment.
  • 29. 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 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).
  • 30. 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).
  • 31. A positive family history may also be obtained in some cases. 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.
  • 32. 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+). R.R. Kussmaul’s breathing in metabolic acidosis, tachypnea in renal failure. B.P. cause & result may be severely elevated (HTN emergency)
  • 33. 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.
  • 34. 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)
  • 35. 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.
  • 36. 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.
  • 37. 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.
  • 38. 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).
  • 39. 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.
  • 40. 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.
  • 41. 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). Splenomegaly may be observed in SLE. • Palpable kidneys : occurs in APKD or renal tumour, or occasionally in amyloidosis. Abdominal aortic aneurysm (associated with renovascular disease and retroperitoneal fibrosis). Renal bruits +/ − femoral bruits: associated with renovascular disease.
  • 42. 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.
  • 43. GN complications e.g. Uraemia can be associated with encephalopathy (i.e. impairment of conciousness +/ − confusion). 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.
  • 44. Vasculitides (particularly Churg - Strauss syndrome) are associated with peripheral neuropathy or mononeuritis multiplex. Some patients with SLE have neuropsychiatric features, including poor memory 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).