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Saudi Journal of Kidney Diseases and Transplantation
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EDITORIAL Table of Contents   
Year : 2005  |  Volume : 16  |  Issue : 3  |  Page : 282-287
Lung Disease in Relation to Kidney Diseases

1 Division of Internal Medicine, Department of Medicine, King Fahad National Guard Hospital, Riyadh, Saudi Arabia
2 Division of Nephrology, Department of Medicine, King Fahad National Guard Hospital, Riyadh, Saudi Arabia

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How to cite this article:
Hassan IS, Ghalib MB. Lung Disease in Relation to Kidney Diseases. Saudi J Kidney Dis Transpl 2005;16:282-7

How to cite this URL:
Hassan IS, Ghalib MB. Lung Disease in Relation to Kidney Diseases. Saudi J Kidney Dis Transpl [serial online] 2005 [cited 2023 Jan 30];16:282-7. Available from: https://www.sjkdt.org/text.asp?2005/16/3/282/32855

   Introduction Top

Physiologically, the lungs and kidneys are intricately related, not least as homeostatic organs controlling the cellular electrolyte and acid-base status that guarantee the best microenvironment for cellular function. Per­ceptually, pulmonary abnormalities may arise as a direct consequence of renal disease (primary consequences) or through generalized systemic processes that specifically involve both organ systems concomitantly. The former group is the subject of this article. [1],[2],[3] These consequences may be classified on a patho-physiologiocal basis based on the resultant functional de­rangement in renal homeostatic mechanisms [Table - 1]. The latter, so-called pulmonary renal syndrome, is classically exemplified by the vasculitidis, granulomatous diseases, intoxi­cations and sepsis [Table - 2]. Pulmonary complications of dialysis and transplantation are secondary consequences and will not be discussed.

   Pulmonary Edema Top

Pulmonary edema in the setting of renal disease may be multifactorial underlying the various pathogenetic mechanisms responsible for its clinical occurrence. It can generally be classified as primarily renal (renal pulmonary edema/renal asthma/non-cardiogenic pulmo­nary edema) or secondary to the renal cardiac consequences. Renal pulmonary edema is classically related to excess extracellular fluid accumulation subsequent to impaired water and solute excretion e.g. fluid overload secondary to acute or chronic renal failure or secondary to renal artery stenosis (RAS). A less common form of primary renal pulmonary edema that is not related to fluid overload is microvascular pulmonary edema resulting from an increased pulmonary capillary permeability possibly augmented by an associated reduction in plasma oncotic pressure. The renal cardiac consequences are exemplified by secondary hypertensive, coronary, anemic or uremic cardiomyopathy. Clearly, the diagnostic work­up and management will be directed by the medical history and clinical examination and investigation findings. Uremic cardiomyopathy is a diagnosis of exclusion and is classically improved by intensive renal replacement therapy or transplantation. [4],[5]

One cause of renal pulmonary edema that merits expanding on is RAS. Atherosclerotic RAS is a recognized cause of both acute and chronic "congestive cardiac failure". The former is generally described as "flash pulmonary edema" [6] and the latter presents as the "apparent heart failure". [7] The hallmark of pulmonary edema in RAS is a substantially increased renin secretion from the juxta glomerular apparatus of an ischemic kidney. This and through the angiotensin-aldosterone axis, leads to increased water and salt retention by the affected kidney, which a diseased contralateral kidney is unable to handle. Presence of any of the following is a pre-requisite for these pathophysiological abnormalities to take place: a) significant bilateral renal artery stenoses and b) unilateral renal artery ste­nosis with absent or diseased contralateral kidney.

The pulmonary edema that ensues is a consequence of fluid overload rather than left ventricular dysfunction per se. The usual trigger is the introduction of angiotensin converting enzyme inhibitor or angiotensin II receptor blocker therapy. Occasionally, no actual trigger is identifiable. The clinical clues for RAS as a cause of this complication include: associated hypertension which may be difficult to control, renal impairment (rever­sible if related to angiotensin converting enzyme inhibitor therapy), presence of wide­spread vascular disease e.g. carotid atheroma, coronary artery disease, peripheral limb ischemia, preserved left ventricular function on echocardiography and inequality of kidney size on ultrasound (more than 1.5 cm differ­ence). Ultra sound Doppler study, magnetic resonance angiography, tomographic angio­graphy or digital subtraction angiography of the renal arteries will help confirm the diagnosis.

The best management strategy for RAS is a controversial matter. [8],[9] Angioplasty with stenting or surgical correction are thera­peutically equivalent. [10] Favorable outcome parameters for these techniques include discrete proximal stenotic lesions and relatively pre­served kidney size. In such patients, revasculari­zation is usually followed by dramatic natriuresis (and significant drop in the atrial natriuretic factor) and resolution of the pulmonary edema. [7] Indeed, improvement or clearance of pulmonary edema seems to be a more consistent beneficial outcome to revascularization when compared to what is usually seen after such interventions in patients with RAS-associated refractory hypertension or renal impairment.

   Pulmonary Function Top

Multiple mechanical and hemodynamic derangements in pulmonary function are recognized in patients with renal disease [11],[12] Most derangements are sub clinical. Abnor­malities in lung function include alterations in respiratory dynamics, muscle functions and gas transfer. The latter seems to be the most serious, and is probably the result of pulmonary fibrosis consequent to chronic or recurrent pulmonary edema, uremic pneumonitis and/ or pulmonary microcalcification. Pulmonary metastatic calcification subsequent to secondary hyperparathyroidism occurs primarily in the alveolar septa and to a lesser extent in the arterial and bronchial walls. [12],[13] Up to 60% of patients with end-stage renal disease (ESRD) on dialysis may develop this complication. [12],[13] The majority of them are however, asympto­matic with no apparent chest X-ray changes. In the few who become symptomatic, a high­resolution computerized lung scan followed by a radionuclide bone scan will confirm the presence of calcific lung deposits. [14] Parathy­roidectomy, use of the new vitamin D analogues or transplantation may help reverse the abnormality. [15] Extra-pulmonary restrictive lung disease, primarily related to uremic fibrinous pleuritis (fibrothorax) that occa­sionally warrants surgical decortications, [16] or secondary to uremic phrenic neuropathy with diaphragmatic paralysis, is a recognized com­plication of chronic renal failure (CRF). [17] Rarely, a hugely enlarged mediastinal para­thyroid cyst may cause tracheal obstruction and stridor. [18]

Another recently documented complication of CRF is central and obstructive sleep apnea, which tends to improve with dialysis or transplantation. [19],[20]

   Pleural Effusion Top

These are common in patients with CRF. They can be secondary to fluid overload, renal cardiac disease, pulmonary embolism or tuber­culous infection [Table - 1]. However, pleural effusions primarily related to uremia may also be seen. [21] These may be unilateral or bilateral and range in size from small to massive. [22] They may macroscopically be clear or more commonly sero-sanguineous or frankly hemor­rhagic. Protein content is variable with the effusion being more frequently exudative. Cellularity is usually lymphocyte predominant. Uremic pleural effusion is diagnosed by excluding other possible etiologies. Response to renal replacement is not invariable. [1],[23]

A urinothorax is a rare complication of obstructive, inflammatory or malignant renal disease. [24] A fistula or communication between the collecting ducts and the thoracic cavity allows for urine to accumulate in the pleural space. Such pleural effusions are classically transudative, with a low pH, have a pleural creatinine to serum creatinine ratio of more than one and smell of urine [24].

   Pneumonia Top

Pneumonia is reported to complicate at least a third of all episodes of acute renal failure. [25] Similarly, CRF and the nephrotic syndrome are associated with profound immune deficits that predispose [26] patients with these conditions to infections. [26],[27] Immune deficits involve both the humoral and cellular arms of the immune response. [28] Infection is reported to be the second leading cause of death among patients with ESRD. In a retrospective data analysis, the overall pulmonary infectious mortality was 14-16 fold higher in dialysis patients compared to the general population. Infectious complications include viral, bacterial and fungal pathogens. [26],[27] An important bacterial infection in patients with CRF is tuberculosis (6.9-52.5 times higher risk). In a study in two renal units in two large hospitals in Jeddah, Saudi Arabia, pulmonary tuberculosis was diagnosed in 10 of 17 patients with this disease. [29],[30] Presentation of tuberculosis in patients with CRF is usually nonspecific and is generally masked by the associated uremic symptoms. However, persistent fever and unexplained hypercalcemia are clues to the presence of tuberculosis. [31] Tuberculin skin testing and chemoprophylaxis are recommended in patients with ESRD.

   Pulmonary Embolism Top

A hyper-coagulable state is one of the hall­ marks of the nephrotic syndrome. [32],[33] Renal vein thrombosis may complicate the nephrotic syndrome, classically of the membranous type. It may be unilateral or bilateral and may extend to involve the inferior vena cava. Thrombosis is usually insidious and asymptomatic or occasionally acute with severe flank pains and hematuria. Pulmonary embolism and infarction are demonstrable in up to a third of patients by perfusion scanning. Ultra sound Doppler study, magnetic resonance angiography and inferior vena cavogram with selective renal venography will help establish the diagnosis. [34],[35] Acute renal vein thrombosis, especially if bilateral and is associated with significant renal impairment warrants surgical thrombectomy or a trial of local thrombolytic therapy; otherwise anticoagulation with heparin and warfarin is adequate. [36],[37] The incidence of deep venous thrombosis, other than that of the renal veins, is also increased in patients with the nephrotic syndrome. The role of prophylactic anticoagulation in such patients is unclear.

   References Top

1.Vermeire P, De Backer. Renal Disease: Respiratory Effects of systemic Disease. Respiratory Medicine. New York. Saunders Company Limited, 1995;1622-9.  Back to cited text no. 1    
2.Prakash UBS. Renal Diseases. Textbook of Pulmonary Diseases. Philadelphia, Lippincott­Raven Publishers 1998;1111-32.  Back to cited text no. 2    
3.Rodriguez-Roisin R, Barbera JA. Pulmonary Complications of Abdominal Disease. Textbook of Respiratory Medicine. New York. Saunders Company Limited, 2000, 2267-84.  Back to cited text no. 3    
4.Hung J, Harris PJ, Uren RF, Tiller DJ, Kelly DT. Uremic cardiomyopathy-effect of hemodialysis on left ventricular function in end-stage renal failure. N Engl J Med. 1980; 302(10):547-51.  Back to cited text no. 4    
5.Burt RK, Gupta-Burt S, Suki WN, Barcenas CG, Ferguson JJ, Van Buren CT. Reversal of left ventricular dysfunction after renal transplantation. Ann Intern Med 1989; 111(8):635-40.  Back to cited text no. 5    
6.Walker F, Walker DA, Nielsen M. Flash pulmonary oedema. Lancet 2001;358:556.  Back to cited text no. 6  [PUBMED]  [FULLTEXT]
7.Missouris CG, Belli AM, MacGregor GA. "Apparent" heart failure: a syndrome caused by renal artery stenoses. Heart 2000; 83: 152-5.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]
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9.Ives NJ, Wheatley K, Stowe RL, et al. Continuing uncertainty about the value of percutaneous revascularization in athero­sclerotic renovascular disease: a meta analysis of randomized trials. Nephrol Dial Transplant 2003;18:298-304.  Back to cited text no. 9  [PUBMED]  [FULLTEXT]
10.Weibull H, Bergqvist D, Bergentz SE, Jonson K, Hulthen L, Manhem P. Per­cutaneous transluminal renal angioplasty versus surgical reconstruction of atherosclerotic renal artery stenosis: a prospective randomized study. J Vasc Surg 1993;18:841-852.  Back to cited text no. 10    
11.Prezant DJ. Effect of uremia and its treatment on pulmonary function. Lung 1990;168(1):1-14.  Back to cited text no. 11    
12.Bush A, Gabriel R. Pulmonary function in chronic renal failure: effects of dialysis and transplantation. Thorax 1991;46(6):424-8.  Back to cited text no. 12    
13.Justrabo E, Genin R, Rifle G. Pulmonary metastatic calcification with respiratory insufficiency in patients on maintenance haemodialysis. Thorax 1979;34:384-8.  Back to cited text no. 13  [PUBMED]  
14.Faubert PF, Shapiro WB, Porush JG, et al. Pulmonary calcification in hemodialyzed patients detected by technetium-99m diphos­phonate scanning. Kidney Int 1980;18:95-102.  Back to cited text no. 14  [PUBMED]  
15.Cunningham J. Achieving therapeutic targets in the treatment of secondary hyperparathy­roidism. Nephrol Dial Transplant 2004; Suppl 5:9-14.  Back to cited text no. 15    
16.Gilbert L, Ribot S, Frankel H, Jacobs M, Mankowitz BJ. Fibrinous uremic pleuritis: a surgical entity. Chest 1975;67:53-6.  Back to cited text no. 16  [PUBMED]  [FULLTEXT]
17.Zifko U, Auinger M, Albrecht G, et al. Phrenic neuropathy in chronic renal failure. Thorax 1995;50(7):793-4.  Back to cited text no. 17    
18.Landau O, Chamberlain DW, Kennedy RS, Pearson FG, Keshavjee S. Mediastinal para­thyroid cysts. Ann Thorac Surg 1997;63(4):951-3.  Back to cited text no. 18    
19.Kimmel PL, Miller G, Mendelson WB. Sleep apnea syndrome in chronic renal disease. Am J Med 1989;86:308-14.  Back to cited text no. 19  [PUBMED]  
20.Mendelson WB, Wadhwa NK, Greenberg HE, Gujavarty K, Bergofsky E. Effects of hemo­dialysis on sleep apnea syndrome in end-stage renal disease. Clin Nephrol 1990;33(5):247-51.  Back to cited text no. 20    
21.Nidus BD, Matalon R, Cantacuzino D, Eisinger RP. Uremic pleuritis - a clinico-pathological entity. N Engl J Med 1969;281(5):255-6.  Back to cited text no. 21    
22.Yoshii C, Morita S, Tokunaga M, et al. Bilateral massive pleural effusions caused by uremic pleuritis. Intern Med 2001; 40(7):646-9.  Back to cited text no. 22    
23.Berger HW, Rammohan G, Neff MS, Buhain WJ. Uremic pleural effusion. A study in 14 patients on chronic dialysis. Ann Intern Med 1975;82(3):362-4.  Back to cited text no. 23    
24.Hendricks J, Michielson D, Van Schil R, Wyndaele J. Urinothorax: a rare pleural effusion. Acta Chir Belg 2002:102:274-5.  Back to cited text no. 24    
25.McMurray SD, Luft FC, Maxwell DR, et al. Prevailing patterns and predictor variables in patients with acute tubular necrosis. Arch Intern Med 1978;138(6):950-5.  Back to cited text no. 25    
26.Sarnak MJ, Jaber BL. Pulmonary infectious mortality among patients with end-stage renal disease. Chest 2001;120(6):1883-7.  Back to cited text no. 26    
27.Minnaganti VR, Cunha BA. Infections associated with uremia and dialysis. Infect Dis Clin North Am 2001;15(2):385-406.  Back to cited text no. 27    
28.Cohen G, Haag-Weber M, Horl WH. Immune dysfunction in uremia. Kidney Int Suppl 1997;62:S79-82.  Back to cited text no. 28    
29.Shohaib SA, Scrimgeour EM, Shaerya F. Tuberculosis in active dialysis patients in Jeddah. Am J Nephrol 1999;19(1):34-7.  Back to cited text no. 29    
30.Hussein MM, Mooij JM, Roujouleh H. Tuberculosis and chronic renal disease. Semin Dial 2003;16(1):38-44.  Back to cited text no. 30    
31.Fang HC, Lee PT, Chen CL, Wu MJ, Chou KJ, Chung HM. Tuberculosis in patients with end-stage renal disease. Int J Tuberc Lung Dis 2004;8(1):92-7.  Back to cited text no. 31    
32.Llach F. Hypercoagulability, renal vein thrombosis, and other thrombotic compli­cations of nephrotic syndrome. Kidney Int 1985;28:429-39.  Back to cited text no. 32  [PUBMED]  
33.Rabelink TJ, Zwaginga JJ, Koomans HA, Sixma JJ. Thrombosis and hemostasis in renal disease. Kidney Int 1994;46:287-96.  Back to cited text no. 33  [PUBMED]  
34.Avasthi PS, Greene ER, Scholler C, Fowler CR. Noninvasive diagnosis of renal vein thrombosis by ultrasonic echo-Doppler flowmetry. Kidney Int 1983;23(6):882-7.  Back to cited text no. 34    
35.Rahmouni A, Jazaerli N, Radier C, et al. Evaluation of magnetic resonance imaging for the assessment of renal vein thrombosis in the nephrotic syndrome. Nephron 1994; 68(2):271-2.  Back to cited text no. 35    
36.Burrow CR, Walker WG, Bell WR, Gatewood OB. Streptokinase salvage of renal function after renal vein thrombosis. Ann Intern Med 1984;100(2):237-8.  Back to cited text no. 36    
37.Lam KK, Lui CC. Successful treatment of acute inferior vena cava and unilateral renal vein thrombosis by local infusion of recombinant tissue plasminogen activator. Am J Kidney Dis 1998;32(6):1075-9.  Back to cited text no. 37    

Correspondence Address:
Imad Salah Ahmed Hassan
Consultant, Division of Internal Medicine, Department of Medicine, King Fahad National Guard Hospital, P.O. Box 22490, Riyadh 11426
Saudi Arabia
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Source of Support: None, Conflict of Interest: None

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