1. History Salient Features Physical Exam
A 50 y/o was referred for evaluation of azotemia.
10 yrs ago, he experienced sudden onset of pain on his right big toe. His serum uric acid was elevated. He was diagnosed to have gout and was prescribed medication but he was poorly compliant. The gouty attacks recurred lately hence, he decided to undergo thorough check-up. He denies dysuria, flank pain or hesitancy. He has nocturia.
BP is 120/70
Obese
numerous tophi in his metacarpo-phalangea l elbow joint
no edema
A 50 y/o obese male with longstanding hyperuricemia
Patient experiences nocturia but there is no dysuria, flank pain or hesitancy, and edema
BP is 120/70
Numerous tophi in his metacarpo-phalangeal elbow joint

2. Clinical Impression Gouty nephropathy
Patients with prolonged forms of hyperuricemia are predisposed to a more chronic tubulointerstitial disorder
Distinctive feature: presence of crystalline deposits of uric acid and monosodium urate salts in kidney parenchyma
Clinically, gouty nephropathy is an insidious cause of renal insufficiency.
Early in its course GFR may be near normal despite focal morphologic changes in medullary and cortical interstitium and diminished urinary concentrating ability
- These deposits not only causes intrarenal obstruction but also incite an inflammatory response leading to lymphocytic infiltration, foreign-body giant cell reaction and eventual fibrosis
Gout is a metabolic disease resulting from an increased body pool of urate due to an overproduction or underproduction of uric acid. It is characterized by episodic arthritis due to the deposition of monosodium urate crystals in joints and connective tissue tophi (just as seen in our patient), and the risk for deposition in the kidney interstitium or uric acid nephrolithiasis.
Patients with prolonged forms of hyperuricemia (just as in the case of our patient who was diagnosed to have gout 10 years ago, was poorly compliant with his medications and now experiencing a recurrence of gouty attacks) are predisposed to a more chronic tubulointerstitial disorder, often referred to as gouty nephropathy, which is also known as chronic uric acid nephropathy.
The distinctive feature of this type of disease is the presence of crystalline deposits of uric acid and monosodium urate salts in the kidney parenchyma. These deposits not only causes intrarenal obstruction but also incite an inflammatory response leading to lymphocytic infiltration, foreign-body giant cell reaction and eventual fibrosis.
Clinically, gouty nephropathy is an insidious cause of renal insufficiency. Despite the focal morphologic changes in the medullary and cortical interstitium, proteinuria and diminished urinary concentrating ability, the glomerular filtration rate may be near normal.

3. Algorithm/Sequence of Events
Renal Deposition of Urates
Pelvic Calculi
Parenchymal Urate
(microtophi)
Tubular Uric Acid
(obstruction)
Gout
Renal Insufficiency

4. Differential Diagnosis
Diabetic Nephropathy
Kimmelstiel-Wilson syndrome
a progressive kidney disease caused by angiopathy of capillaries in the kidney glomeruli
characterized by nephrotic syndrome and diffuse glomerulosclerosis.

5. Spectrum of Disease Diagram
Lower testing threshold
Upper testing threshold
Pretest probability
Do nothing. Rule out the disease
Treat the patient without waiting for more information
Do additional diagnostic exams to confirm diagnosis (testing zone)
20 %
70% %
41%