RENAL Flashcards
1
Q
Define Glomerulonephritis
A
An IMMUNOLOGICALLY mediated inflammation of the renal glomeruli
2
Q
Whats the pathophysiology behind glomerulonephritis?
A
MAINLY: deposition of Ant-Ab complexes in the glomeruli
This leads to inflammation and activation of complement and coagulation cascades
The Ant-Ab complexes either form on the spot in the glomeruli (more common) or are deposited from the circulation
3
Q
What are common antigents associated with glomerulonephritis?
A
Bacteria: Streptococcus viridans, Staphylococci
Viruses: HBV, CBV, measles, mumps, EBV.
Protozoa: Plasmodium malariae, Schistosomiasis.
Inflammatory/Systemic Diseases: SLE, vasculitis, cryoglobulinaemia.
Drugs: Gold, Penicillinamine.
Tumours
4
Q
State the 2 main classes of glomerulonephritis
A
Non proliferative and proliferative
5
Q
List the different types of glomerulonephritis
A
NON-PROLIFERATIVE:
- Minimal-change glomerulonephritis
- Membranous glomerulonephritis
- Focal Segmental glomeruloSCLEROSIS
PROLIFERATIVE:
- IgA nephropathy
- MembranoProliferative GlomeruloNephritis (MPGN)
- Focal segmental proliferative glomerulonephritis
- Diffuse proliferative glom.
- Crescentic glomerulonephritis aka Rapidly progressive glomerulonephritis (vasculitic disorders & goodpastures syndrome)
6
Q
What are the PC of glom. ?
A
- Haematuria
- SC oedema
- History of recent infection
- Symptoms of uraemia or renal failure
7
Q
What are the signs OE for glom.
A
- Hypertension
- Proteinuria
- Haematuria (especially in IgA nephropathy)
8
Q
What is the triad of the NEPHROTIC syndrome?
A
Proteinuria > 3.5 g/24 hrs
Low serum albumin < 24 g/L
Oedema
NOTE: due to the hypoalbuminaema, the liver tries to compensate and hence increases the production of lipids causing hyperlipidaemia!
9
Q
What is the triad of the NEPHRITIC syndrome?
A
- Haematuria
- Proteinuria
- Hypertension
Pores in the podocytes are large enough to allow protein AND RBC to pass in the urine.
Red cell casts may also be present - indicating glomerular damage
10
Q
What are the IX for glom. ?
A
BLOODS: FBC U&E's - creatinine LFT's - Albumin * Lipid profile Complement studies Antibodies
URINE
Microscopy
24hr collection - to monitor creatinine clearance and protein
IMAGING:
US- of the Renal Tract to exclude (obstruction)
RENAL Bx
for microscopy
Investigations for associated conditions: HBV, HCV, HIV serology.
11
Q
Which antibodies are you testing for in glom. ?
A
ANA Anti-dsDNA ANCA Anti-GBM Ab Cryoglobulins
12
Q
How can you determine the anatomical origin of macroscopic haematuria based on its presentation?
A
Bladder bleeding = present throughout voiding
Terminal bladder or prostatic bleeding = end of voiding
Urethral bleeding = beggining of voiding.
13
Q
What are red cell casts and what do they indicate?
A
Are RBC that have leaked into renal tubules and clump together forming a cast-like structure which is excreted in the urine
They suggest glomerular pathology/damage.
14
Q
Which is the most common cause of glom.?
A
IgA nephropathy (Berger's disease) is the most common cause Can present at any age
15
Q
What is Henoch-Schonlein Purpura?
How does it present?
A
A small type vasculitides Systemic involvement (compared to Berger's)
It presents with:
Arthritis of large joint
Abdominal pain
Characteristic purpuric rash of the extensor skin surfaces.
“purpura, arthritis, gut symptoms,
glomerulonephritis, IgA deposition”
Is a RF for orchidits and epididymitis
16
Q
Post op diabetic pt gets delirious and agitated
What are you thinking?
A
Hyponatraemia due to fluid overload due to excess dextrose solution given post-op which causes dilutional hyponatraemia resulting in acute delirium.
17
Q
What is diabetic nephropathy?
A
A chronic progressive disease that arises in diabetic pts
It’s characterised by an initial increase in glomerular filtration rate and glomerular BM hypertrophy.
As the disease progresses glomerulosclerosis occurs as a result of accumulation of ECM and destroying the filtering ability of the glomerular membrane.
This allows proteins leakage.
Severe diabetic nepropathy can present with nephrotic syndrome symptoms.
Acute derangement of biochemistry does not occur though.
18
Q
What derangment of biochemistry would excess insulin cause?
A
Hypoglycaemia
Low K+
Due to a shift of K to the IC compartment.
PC: irritable, sweat and can fall into comma.
19
Q
Tubulointerstitial nephritis
A
Due to drug hypersensitivity reactions - penicillin, NSAID’s.
PC: fever, skin rash, painful joints
Blood: HIGH eosinophils
20
Q
Where are eosinophils raised?
A
Allergic responses like: Asthma Drugs Parasitic infections Tissue inflammation
21
Q
What is the most appropriate first IX in renal stones?
A
KUB US or Abdominal US in SBA
of the KUB (Kidneys, Ureters, Bladder)
80% of stones are visible on US
22
Q
What are the most commons kidney stones?
A
Calcium oxalate
23
Q
List the types of kidney stones
A
o Calcium oxalate - MOST COMMON
o Struvite - quite common
o Urate - 5%
o Cysteine - 2%
24
Q
Explain the aetiology/risk factors of urinary tract calculi
A
• Many cases are IDIOPATHIC
Metabolic Causes o Hypercalciuria o Hyperuricaemia o Hypercystinuria o Hyperoxaluria
Infection
o Hyperuricaemia
Drugs
o Indinavir
• RISK FACTORS:
o Low fluid intake
o Structural urinary tract abnormalities (e.g. horseshoe kidney)
25
What is indinavir?
Indinavir (IDV; trade name Crixivan, manufactured by Merck) is a protease inhibitor used as a component of highly active antiretroviral therapy to treat HIV/AIDS.
RF for kidney stones.
26
Recognise the presenting symptoms of urinary tract calculi
* Often ASYMPTOMATIC
* SEVERE loin to groin pain
* Nausea and vomiting
* Urinary urgency, frequency or retention
* Haematuria
27
Recognise the signs of urinary tract calculi on physical examination
* Loin to lower abdominal tenderness
* NO signs of peritonism
* Signs of systemic sepsis if there is an obstruction and infection above the stone
28
What is the main differential to kidney stones in elderly men?
• Leaking AAA is the main differential to consider in older men
29
Identify appropriate investigations for urinary tract calculi
```
• Bloods
o FBC - high WCC if infection
o U&Es - check renal function
o Calcium
o Urate
o Phosphate
```
• Urine
o Dipstick - haematuria is common
o MC&S
• X-Ray KUB
o 80% of kidney stones are radio-opaque
• Intravenous Urography (IVU)
o Allows visualisation of the kidneys and ureters
• Ultrasound
o May show hydronephrosis and hydroureter
• Non-enhanced Spiral CT
o Can also be used to image stones
• Isotope Radiography
o Used to assess kidney function
30
Generate a management plan for ACUTE PRESENTATION of urinary tract calculi
• ACUTE PRESENTATION
o Analgesia
o Bed rest
o Fluid replacement
o Urine collection to try and retrieve any stone that has passed
• NOTE: most stones < 5 mm will pass spontaneously
o An obstructed, infected kidney is an EMERGENCY and should be treated as soon as possible to relieve the obstruction (e.g. by placing a percutaneous
nephrostomy)
31
What is the mx for the removal of calculi?
• REMOVAL OF CALCULI
o Urethroscopy
• A scope is passed into the bladder and up the ureter to visualise the stone
• It can then be removed by a basket or broken up with a laser If the stone cannot be removed, a JJ stent should be placed to allow urine drainage
o Extracorporeal Shock-Wave Lithotripsy (ESWL)
• Non-invasive
• An electromagnetic shockwave is focused onto the calculus to break it up into smaller fragments that can pass spontaneously
o Percutaneous Nephrolithotomy (PCNL)
• Performed for large, complex stones (e.g. staghorn calculi)
• After making a nephrostomy tract, a nephroscope is inserted, which allows disintegration and removal of stones
• TREATMENT OF CAUSE
o Depends on the cause (e.g. parathyroidectomy if hypercalcaemia due to hyperparathyroidism, allopurinol if hyperuricaemia)
• ADVICE
o Increase oral fluid intake
32
Identify possible complications of urinary tract calculi
• Of Stones
o Infection (PYELONEPHRITIS)
o Septicaemia
o Urinary retention
• Of Ureteroscopy
o Perforation
o False passage
• Of Lithotripsy
o Pain
o Haematuria
33
Summarise the prognosis for patients with urinary tract calculi
* GOOD
* However, infection of the calculus could lead to irreversible renal scarring
* Recurrence of about 50% over 5 yrs
34
ASIAN male presents with dusyria, urinary frequency and general malaise the past 6 months.
He noticed blood in the urine recently
Urine: neutrophils
No organisms detected on urine culture
What is this?
Tuberculosis of the renal system
ASIAN = TB !!!!!!
PC: pain in the back, flanks, groin.
Non-specific symptoms: haematuria, frequency, nocturia
ABSENCE of positive urine colture
put PRESENCE of pyuria - neutrophils in the urine
"sterile pyuria"
35
Pt presents with periorbital oedema and mentions a recent throat infection
Urine dip: protein ++ blood ++
Glomerulonephritis
Presenting with nephritic symptoms (haematuria, proteinuria, oedema)
Post throat infection = post streptococcal glomerulonephritis (classic)
36
```
pH = HIGH
co2 = LOW
HCO3- = LOW
po2 = normal
```
What is this?
Metabolic acidosis with respiratory compensation
| Usually caused by hyperventilation = anxiety
37
21yo woman presents with polyuria, polydipsia, nocturia, constipation, polydipsia, general malaise, pain in her left flank
Urine dip is normal
What is the next best investigation?
She has hypercalcaemia
Next best investigation is serum Ca2+ levels.
"bones, stones, groans, moans"
Then measuring PTH to see the CAUSE of hypercalcemia.
38
58yo male pt presents with breathlesness, feeling unwell the past 3 months, nausea, vomiting, difficulty breathing.
Pt mentions he isn't urinating as often.
OE: swollen ankles, bruises on his arms.
What is this? and explain.
What is the next best investigation?
What are the expected results:
This is renal failure
Next investigation: Serum electrolytes, urea and creatinine.
To determine the current level of renal function.
```
Expected results:
HIGH Na+
HIGH K+
HIGH Urea
HIGH Creatinine
```
Renal failure causes uraemia
Uraemia causes non specific symptoms such as nausa, vomiting
Uraemia causes failure to excrete H+ which results in acidosis - this causes hyperventilation and breathlesness.
Oedema results due to the kidney losing its diuretic ability.
Increased kidney impairment leads to reduced haemostatic function causing easy bruising.
Renal failure is often associated with oliguria.
SBA: 3 months is the minimum criterion in the CKD definition.
39
Explain the aetiology/risk factors of CKD
```
• In developed countries it is mainly associated with:
o Age *
o Diabetes mellitus
o Hypertension
o Obesity
o Cardiovascular disease
```
```
• Other risk factors:
o Arteriopathic renal disease
o Nephropathies
o Family history
o Neoplasia
o Myeloma
o Systemic disease (e.g. SLE)
o Smoking
o Chronic use of NSAIDs :(
```
40
Recognise the PC of CKD
* Often ASYMPTOMATIC
* May be an incidental finding of a routine blood or urine test
```
• Symptoms of Severe CKD:
o Anorexia
o Nausea and vomiting
o Fatigue
o Pruritus
o Peripheral oedema
o Muscle cramps
o Pulmonary oedema
• Sexual dysfunction is common
```
41
Recognise the signs of CKD on physical examination
• Physical examination rarely reveals many clues
• May show signs of underlying disease (e.g. SLE)
• May show complications of CKD (e.g. anaemia)
• Signs of CKD:
o Skin pigmentation
o Excoriation marks
o Pallor
o Hypertension
o Peripheral oedema (swollen ankles)
o Peripheral vascular disease (bruises)
42
Identify appropriate investigations for CKD
• Assessment of Renal Function
o Urea - not ideal because it varies massively depending on hydration status and diet
o Creatinine - useful but has limitations. Renal function can drop considerably with minimal change in serum creatinine
o Isotopic GFR - GOLD STANDARD but expensive
• Biochemistry
o Glucose - check for undiagnosed diabetes and diabetic control
o Potassium M raised
o Also check sodium, bicarbonate, calcium, phosphate
```
• Serology
o Antibodies
• ANA - SLE
• c-ANCA - granulomatosis with polyangiitis (Wegener's)
• Anti-GBM - Goodpasture's syndrome
o Hepatitis serology
o HIV serology
```
• Urinalysis
o Check for proteinuria/haematuria
o 24 hr urine collection
o Serum or urine protein electrophoresis - check for multiple myeloma
• Imaging
o Ultrasound - check for structural abnormalities
o CT/MRI
o X-Ray KUB - check for stones
• Renal Biopsy
43
24yo man presents with 4month history of generalised and dull abdo pain along side loin pain.
OE: irregular palpable mass in both flanks, mid systolic click on auscultation
What is this
Whats the next best step
This is classic PKD presentation
Young patient - points towards congenital
Classic PC: abdo pain, loin pain, palpable irregular kidneys
High association with mitral valve disease & berry aneurysms = mid systolic click
Next best step CT/US - will show bilaterally enlarged cystic kidneys.
44
Whats the aetiology of PKD?
85% caused by mutations in PKD1 on chromosome 16
This is a membrane-bound multidomain protein involved in cell-cell and cell-matrix interactions
15% caused by mutations of PKD2 on chromosome 4
45
What's the pathophysiology of PKD?
Proliferative/hyperplastic abnormality of the tubular epithelium
Early on, the cysts are connected to the tubules from which they arise and the fluid content is glomerular filtrate
When cyst diameter >2 mm, they detach from the tubule and the fluid content is derived from secretion of the lining epithelium
With time, the cysts enlarge and cause progressive damage to adjacent functioning nephrons
46
What are the signs OE of PKD?
Abdominal distension
Palpable Enlarged IRREGULAR cystic kidneys
Palpable liver
Hypertension
Signs of chronic renal failure (at late stage)
Mid-systolic click (mitral valve disease)
47
How would you manage a diabetic patient with new onset proteinuria?
Aggresivelly control BP (below 130/80) with ACEi and angiotensin receptor blockers
48
What are the common types of renal cancer?
* Renal clear cell carcinoma (80%) - UNKNOWN CAUSE • Papillary carcinoma (10%) - UNKNOWN CAUSE
* Transitional cell carcinoma (10%) these occur at the renal pelvis
49
What are RF for renal cancer?
• Von Hippel-Lindau disease
- Mutation in the von Hippel-Lindau protein, which causes headaches, balance issues, dizziness, limb weakness, vision problems and high blood pressure
• Tuberous sclerosis
! A rare genetic disease that causes benign tumours to grow in the brain and other organs (e.g. skin, kidneys, lungs, eyes)
• Polycystic kidney disease
• Familial renal cell cancer
• Smoking
• Chronic dialysis
o NOTE: renal cell cancer can cause abnormal LFTs in the absence of liver metastases = Strauffer's Syndrome
50
What is Strauffer's syndrome
Stauffer syndrome is a constellation of signs and symptoms of liver dysfunction that arises due to presence of renal cell carcinoma (and rarely other malignancies)
51
Recognise the presenting symptoms of renal cell cancer
• Renal Cell Carcinoma
o Usually present LATE
o Asymptomatic in 90%
o Triad of Symptoms:
• Haematuria
• Flank pain
• Abdominal mass
• Transitional Cell Carcinoma
o Presents EARLIER with haematuria
• Systemic Signs of Malignancy
o Weight loss
o Malaise
o Paraneoplastic syndromes (e.g. fever, hypercalcaemia, polycythaemia)
52
What is paraneoplastic syndrome?
A paraneoplastic syndrome is a syndrome (a set of signs and symptoms) that is the consequence of cancer in the body, but unlike mass effect, is not due to the local presence of cancer cells.
EG: fever, hypercalcaemia, polycythaemia)
53
Recognise the signs of renal cell cancer on physical examination
```
• Palpable renal mass
• Hypertension
• Plethora of blood
• Anaemia
• A left-sided tumour can obstruct the left testicular vein as it joins the left renal vein, and cause a left-
sided varicocoele
```
54
Identify appropriate investigations for renal cell cancer
• Urinalysis
o Haematuria
o Cytology
```
• Bloods
o FBC
o U&Es
o Calcium
o LFTs
o High ESR (in 75%)
```
Abdominal Ultrasound *
o Best first-line investigation
o Can distinguish between solid masses and cystic structures
• CT/MRI
o Useful for staging
• Staging system: Robson Staging
55
Whats the staging system for renal cancer?
```
Robson staging
(done by MRI/CT)
```
56
Acute hyperuricaemic nephropathy
What is it
How does it present
Common finding in pts suffering from hyperuricaemia
Occurs in pts with high cell turnover like myeloproliferative disorders or following chemotherapy
Uric acid crystallizes in the renal system causing obstructions which can manifest as flank pain, oliguria, HTN, oedema, uraemic symptoms (SOB)
57
67yo female pt is brought to A&E after a fall at home
Urine dip: glucose ++, nitrates ++, leukocytes ++, blood ++
BP: low
what is this
UTI
elderly, female, diabetic = classic
Severe infections can cause sepsis, hypovolaemia and collapse.
No ketones in urine dip = not DKA
58
Define UTI
The presence of a pure growth of >10^5 organisms per mL of fresh MSU
NOTE: 1/3 of women have a negative MSU
59
What are the sub-classifications of a UTI
Lower UTI - affecting urethra, bladder or prostate (urethritis, cystitis, prostatitis)
Upper UTI - affecting the renal pelvis (pyelonephritis)
Uncomplicated UTI - normal renal tract and function
Complicated UTI - abnormal renal/genitourinary tract, voiding difficulty/obstruction, reduced renal function, impaired host defences, virulent organism ( S aureus)
60
Which organisms causes UTI's most commonly
E Coli
61
What organisms cause UTI
Staphylococcus saprophyticus
Proteus mirabilis
Enterococci
62
Which atypical organisms cause UTI's
Atypical organisms that can cause UTI (usually in immunocompromised individuals):
Klebsiella
Candida albicans
Pseudomonas aeruginos
63
What are the RF for UTI's
```
FEMALE
Sexual intercourse
Exposure to spermicide
Pregnancy
Menopause
Immunosuppression
Catheterisation
Urinary tract obstruction
Urinary tract malformation
```
64
Recognise the presenting symptoms of urinary tract infections
```
CYSTITIS
Frequency
Urgency
Dysuria
Haematuria
Suprapubic pain
```
```
PROSTATITIS
Flu-like symptoms
Low backache
Few urinary symptoms
Swollen or tender prostate on PR
```
```
ACUTE PYELONEPHRITIS
High fever
Rigors
Vomiting
Loin pain/ tenderness
Oliguria (AKI)
```
65
Signs of UTI OE
```
Fever
Abdominal or loin tenderness
Foul-smelling urine
Distended bladder (occasionally)
Enlarged prostate (if prostatitis)
```
66
Identify appropriate investigations for urinary tract infection
• Urine Dipstick
o Positive leucocyte ++ esterase and nitrites ++
• Urine Microscopy
o Presence of leucocytes indicates infection
• Urine Culture
o To exclude diagnosis or if the patient failed to respond to empirical antibiotics
• Ultrasound
o Rule out obstruction
```
• Bloods
o FBC
o U&Es - check renal function
o CRP
o Blood cultures - if systemically unwell and risk of urosepsis
```
67
Generate a management plan for urinary tract infection
• Empirical treatment of uncomplicated UTI: TRIMETHOPRIN or NITROFURANTOIN*
o Treat for 3-6 days
o NOTE: men with UTI may need a longer course of antibiotics
• Alternative Treatments: Co-amoxiclav or Cefalexin
• Prophylactic antibiotics may be used in certain circumstances (e.g. recurrent cystitis
associated with sexual intercourse)
68
Identify possible complications of urinary tract infection
```
• Ascending infection can lead to:
o Pyelonephritis
o Perinephric and intrarenal abscess
o Hydronephrosis or pyonephrosis
o AKI
o Sepsis
```
• Prostatic involvement (e.g. prostatitis) in men with UTIs is common
69
What is the most common cause of glomerulonephritis in young adults?
Minimal change nephropathy
70
65yo male pt presents with 2week haematuria
He is a chronic smoker
He has been trying out some chinese herb weight loss medicines
He lost some weight recently
What is this?
Bladder cancer - classic.
RF: smoking*, dyes*, chinese herbal weight loss remedies (aristolochic acid)
PAINLESS HAEMATURIA + WEIGHT LOSS
71
Define AKI
An abrupt loss of kidney function resulting in the retention of urea and other nitrogenous waste products and the dysregulation of extracellular volume and electrolytes.
72
What are the causes of AKI?
• Pre-Renal (90%)
o Hypovolaemia (e.g. haemorrhage, severe vomiting)
o Heart failure
o Cirrhosis
o Nephrotic syndrome
o Hypotension (e.g. shock, sepsis, anaphylaxis)
o Renal hypoperfusion (e.g. NSAIDs, ACE inhibitors, ARBs, renal artery stenosis)
• Intrinsic Renal
o Glomerular - glomerulonephritis, haemolytic uraemic syndrome
o Tubular - acute tubular necrosis
o Interstitial - acute interstitial nephritis (e.g. NSAIDs, autoimmune)
o Vasculitides (e.g. Wegener's granulomatosis)
o Eclampsia
```
• Post-Renal (due to obstruction)
o Calculi
o Urethral stricture
o Prostatic hypertrophy or malignancy
o Bladder tumour
```
73
What are the RF for AKI?
```
o Age
o Chronic kidney disease
o Comorbidities (e.g. heart failure)
o Sepsis
o Hypovolaemia
o Use of nephrotoxic medications
o Emergency surgery (AAA rupture)
o Diabetes mellitus
```
74
What are the PC of AKI
• Depends on underlying CAUSE
• Oliguria (minimal urination) /anuria (NO urination)
o NOTE: abrupt anuria suggests post-renal obstruction
• Nausea/vomiting
• Dehydration
• Confusion
75
Recognise the signs of AKI on physical examination
* Hypertension
* Distended bladder
* Dehydration - postural hypotension
* Fluid overload (in heart failure, cirrhosis, nephrotic syndrome) - raised JVP, pulmonary and peripheral oedema
* Pallor, rash, bruising (vascular disease)
76
Identify appropriate investigations for AKI
```
• Urinalysis
o Blood - suggests nephritic cause
o Leucocyte esterase and nitrites - UTI
o Glucose
o Protein
o Urine osmolality
```
```
• Bloods
o FBC
o Blood film
o U&Es
o Clotting
o CRP
```
o Immunology
• Serum immunoglobulins and protein electrophoresis - for multiple myeloma
- Also check for Bence-Jones proteins in the urine
• ANA - associated with SLE
! Also check anti-dsDNA antibodies (high in active lupus)
• Complement levels - low in active lupus
• Anti-GBM antibodies - Goodpasture's syndrome
• Antistreptolysin-O antibodies - high after Streptococcal infection
o Virology - check for hepatitis and HIV
• Ultrasound
o Check for post-renal cause
o Look for hydronephrosis
• Other Imaging
o CXR M pulmonary oedema
o AXR M renal stones
77
Generate a management plan for AKI
• Treat the cause
• FOUR main components to management:
o Protect patient from hyperkalaemia (calcium gluconate) o Optimise fluid balance
o Stop nephrotoxic drugs
o Consider for dialysis
• Monitor serum creatinine, sodium, potassium, calcium, phosphate and glucose
• Identify and treat infection
• Urgent relief of urinary tract obstruction
• Refer to nephrology if intrinsic renal disease is suspected
• Renal Replacement Therapy (RRT) considered if:
o Hyperkalaemia refractory to medical management
o Pulmonary oedema refractory to medical management o Severe metabolic acidaemia
o Uraemic complications
78
Identify possible complications of AKI
* Pulmonary oedema
* Acidaemia
* Uraemia
* Hyperkalaemia
* Bleeding
79
What do renal artery bruits indicate?
Renal artery stenosis
80
How does renal artery stenosis manifest?
Unmanegable HTN
| Exacerbationon ACEi - severe HTN, kidney failure.
81
What is a good marker for monitoring/screening for diabetic neprhopathy??
Microalbumin detection in the urine
Increase in microalbumin in the urine menas the pt is at greater risk for furhter renal famage.
Not detectable with urine dip.
82
```
Known chronic renal failure pt
OE:
High Phosphate
High Creatinine & Urea
Low Ca2+
```
What is this?
2' hyperparathyroidism is associated with renal failure
High phosphate + Low ca
"increased secretion of PTH secondary to hypocalcaemia"
83
Classic presentation of acute pyelonephritis
```
High fever
Rigors
Vomiting
Flank pain
Oliguria
```
Due to a gram -ve infection
Poorly controlled diabetes is a risk for this
Gas on CT = parenchymal infection results in gas accumulation
