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This document presents the case of a 47-year-old man who presented with facial puffiness, joint pain, fatigue, and renal dysfunction. He was diagnosed with hypertension previously. Differential diagnoses included systemic lupus erythematosus, Wegener's granulomatosis, and Goodpasture's disease. Investigations showed proteinuria, elevated creatinine, and a positive ANA. He was started on treatments including steroids, hydroxychloroquine, and methotrexate. The discussion section reviews how various systemic diseases can manifest with renal involvement.
This document presents the case of a 47-year-old man who presented with facial puffiness, joint pain, fatigue, and renal dysfunction. He was diagnosed with hypertension previously. Differential diagnoses included systemic lupus erythematosus, Wegener's granulomatosis, and Goodpasture's disease. Investigations showed proteinuria, elevated creatinine, and a positive ANA. He was started on treatments including steroids, hydroxychloroquine, and methotrexate. The discussion section reviews how various systemic diseases can manifest with renal involvement.
This document presents the case of a 47-year-old man who presented with facial puffiness, joint pain, fatigue, and renal dysfunction. He was diagnosed with hypertension previously. Differential diagnoses included systemic lupus erythematosus, Wegener's granulomatosis, and Goodpasture's disease. Investigations showed proteinuria, elevated creatinine, and a positive ANA. He was started on treatments including steroids, hydroxychloroquine, and methotrexate. The discussion section reviews how various systemic diseases can manifest with renal involvement.
SUPERVISOR: DR. BEN EGHAN 12/15/2010 TGBTG HISTORY Forty-seven year old man, known alcoholic with 7 pack years of smoking cigarettes was well until 3 months ago when he felt he easily became fatigued and breathless with activities he could previously undertake with ease. At the same time he experienced occasional dizziness and regular palpitations. TGBTG HISTORY Within a week he noticed he had early morning facial puffiness which resolved during the day, as well as bilateral painless pedal swelling, abdominal distention and a sense of early satiety. He experienced orthopnoea but had no paroxysmal nocturnal dyspnoea. TGBTG HISTORY . In addition, he had anorexia, metallic taste with sialorrhea, painful swollen joints, migratory in nature and bone pain especially of both knees. Initially he resorted to herbal medication and drank herbal mixtures prepared from mahogany( Meliacae family) for at least 2 weeks with no improvement. TGBTG HISTORY He reported at KATH and was diagnosed with hypertension and discharged with antihypertensives(unspecified). Four days later he was brought in with an acute exacerbation of breathlessness with cough productive of brownish sputum and was subsequently admitted. TGBTG HISTORY Systemic review revealed that he had pruritus, nocturia, frothy urine, hesitancy. He had no fever, seizures, jaundice and haematuria. Past medical history: He has no history of diabetes mellitus, sickle cell disease,pyelonephritis, admissions and blood transfusions. TGBTG HISTORY He has never had any radiologic procedure with radiocontrast medium. No known history of syphilis, hepatitis B and HIV. He has a history of multiple bee stings. He has had recurrent episodes of epistaxis since childhood.
TGBTG HISTORY Drug history: He takes Ibuprofen frequently for musculoskeletal pain. No history of recent administration of procainamide, hydralazine, quinidine and isoniazid. Family history: There is a family history of hypertension. No known family history of diabetes or kidney disease.
TGBTG HISTORY Social History: He has been divorced for about a year. He has six children and is a farmer. He stopped smoking cigarette and drinking alcohol about 4 months ago. He is registered with the NHIS.
TGBTG EXAMINATION On examination was a middle aged man who looked unwell and was lying propped up in bed. He was conscious, alert and well hydrated. He had a hypopigmented rash on the malar eminences. He was pale, anicteric with no palpable lymph nodes. He had bilateral, pitting and non-tender pedal oedema up to the knee. No clubbing, Dupuytrens contracture, spider angioma, palmar erythema or leuconychia. TGBTG EXAMINATION CVS: Pulse was 80bpm, regular, of good volume and non-collapsing. BP: 140/85mmHg Apex beat was in the left 6 th intercostals space, a centimeter lateral to the mid- clavicular line. He had no parasternal heaves nor thrills. Heart sounds S1 and S2 were present and normal together with a third heart sound. He did not have a murmur.
TGBTG EXAMINATION Respiratory: He had no chest deformities, chest expansion was equal. Tactile fremitus was normal. Air entry was adequate, breath sounds were bronchial with expiratory wheezes bilaterally.
TGBTG EXAMINATION Abdomen: Full and moved with respiration. No areas of tenderness on palpation. Liver span 15cm, soft smooth and nontender. Spleen and kidneys not palpable. Percussion note was tympanic. CNS: No defects in cognition, memory, cranial nerves and motor system.
TGBTG DISCUSSION POINTS TGBTG RENAL MANIFESTATIONS OF SYSTEMIC DISEASE The kidney is often involved in systemic disease. Renal dysfunction also presents with systemic manifestations of disease. Eg. Heart failure Acute Kidney Injury Chronic Kidney Disease Pericarditis CKD Hypertension TGBTG SLE Renal component part of SLE even if not clinically obvious.(lupus nephritis) Immune complex deposition in GBM activation of complement inflammatory cell invasion. Presents as proteinuria( might be in nephrotic range), haematuria and glomerular casts. TGBTG References Renal Manifestations of systemic disease(2009) PatientUK retrieved 15 th November,2010 from http://www.patient.co.uk/doctor/Renal-Manifestations-of- Systemic-Disease.htm Longmore M., Wilkinson I., Turmezei T. Cheung K.C,(2008) Oxford Handbook of Clinical Medicine, Oxford UK. Oxford University Press. KUMAR V, ABBAS K.A, FAUSTO N (2005).PATHOLOGIC BASIS OF DISEASE. ELSEVIER SAUNDERS, PHILADELPHIA Boon A.N,Colledge R.N, Walker B.R(2005).DAVIDSONS PRINCIPLES AND PRACTICE OF MEDICINE. ELSEVIER SAUNDERS, PHILADELPHIA
TGBTG Closing thought.. The aim of medicine is to prevent disease and prolong life, the ideal of medicine is to eliminate the need of a physician. William J. Mayo (1861 - 1939)
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TGBTG DIABETIC NEPHROPATHY The most common systemic manifestation of systemic disease is diabetic nephropathy. Commonly presents after about 10yrs of DM. Starts as microalbuminuria (30-300mg/day) Progresses to frank albuminuria(>300mg/day) Hyperglycaemia alters cytokine activity. Initially,hyperfiltration,mesangial expansion, Bowman C thickening, glomerular hypertrophy.: RAAS, endothelin activation, PKC, TGF-B and abnormal polyol metabolism. Rx: Glucose control, control BP and use ACEi even in normotensives. TGBTG HYPERTENSIVE NEPHROPATHY of patients presenting with ESRD Nephrosclerosis occurs as a result of ischaemia. Accelerated by malignant hypertension. Hyperfiltration results in intraglomerular hypertension. Patient hypertensive for about 10yrs. Patients present with other complications(eg. HF, retinopathy, MI) Treatment is with ACEi +other antihypertensives. But if RAS, then ACEi is contraindicated.
TGBTG RENAL DYSFUNCTION ASSOCIATED WITH VASCULITIDES Small and medium sized Vasculitides often associated with ANCA. ANCA activates neutrophils, which release mediators with damage to blood vessels. Usually cause RPGN. GFR falls by 50% within 2-3mths. Clinically presents as flu-like symptoms, migratory arthritis, myalgia, fever, anorexia, weight loss, abdominal pain and skin nodules. TGBTG VASCULITIDES PAN: Necrotizing inflammation typically involving renal arteries but sparing pulmonary vessels. Microscopic polyangiitis is similar to PAN but has pulmonary involvement. Wegeners granulomatosis: Classicallyinvolves the nose,sinuses, lungs,and kidneys.(C-ANCA positive. Saddle nose deformity. Churg-Strauss: Allergic asthma , eosinophilia with renal impairment. TGBTG Progressive Systemic Sclerosis Causes renal impairment via microangiopathy or renal crisis. Renal crisis presents in patients with sudden onset of diffuse dermatological involvement. Presents as oliguria, hypertension, headache, rapidly rising creatinine and peripheral oedema. Usually occurs within the first 4yrs of diagnosis. Watch out for it and treat with ACEi. TGBTG MULTIPLE MYELOMA Monoclonal AB from transformed plasma cells. Damage from: light chain deposition, amyloid deposition, hypercalcemia, TLS, cast nephropathy and dehydration. It might be the presenting feature of MM.
TGBTG HUS Most common cause of AKI in children. 85% make full recovery, 15% progress to CKD. Triad of Haemolytic anaemia, thrombocytopenia and renal failure. Infection with E. coli, Shigella, Salmonella, Yersinia, Campylobacter and URTI. GI bleeding and petechiae. Rx is supportive+renal replacement therapy. In severe cases: plasma exchange may be considered. TGBTG SICKLE CELL DISEASE Postmoterm series in adults with SCD found that 20% died of renal failure. The disease causes glomerulopathy with proteinuria, progressive renal insufficiency and ESRF. Papillary necrosis is another mechanism of injury. Children present with hyposthenuria, polyuria and nocturia. Incipient albuminuria is a good marker of disease. Management is by managing SCD to prevent renal complications TGBTG Good pastures Disease Acute glomerulonephritis with pulmonary component( haemoptysis/ pulmonary haemorrhage) Anti-GBM Treatment is supportive, immunosuppressives and plasmapheresis. TGBTG OTHERS Cryoglobinuria Sjgren's syndrome HIV Hepatitis B, syphillis Several other diseases including haematologic, oncologic,immunologic and metabolic diseases have renal manifestations. TGBTG